Differential Diagnosis

Differential
Diagnosis
Differential
Diagnosis
A guide to symptoms and signs of
common diseases and disorders,
presented in systematic form
Alexander D. G. Gunn
MRCOP, DObstRCOO, DPH
Director, University Health Services
University of Reading
United Kingdom
MTaUMITED
International Medical Publishers
Published by
MTP Press Limited
Falcon House
Lancaster, England
Copyright © 1981 A. D. G. Gunn

Softcover reprint of the hardcover 1st edition 1981
First published 1981
All rights reserved. No part of this publication

may be reproduced, stored in a retrieval system,
or transmitted in any form or by any means,
electronic, mechanical, photocopying, recording
or otherwise, without prior permission from the
publishers
British Library Cataloguing in Publication Data
Gunn, Alexander
Differential diagnosis
I. Diagnosis, Differential
I. Title
616.07'5 RC71.5
ISBN-13: 978-94-009-8062-4 e-ISBN -13: 978-94-009-8060-0

DOl: 10.1007/978-94-009-8060-0
Contents
Foreword 7
1 Introduction - how to use this book for reference 9
2 The medical history 13
3 The cardiovascular system 17
4 The respiratory system 37
5 The gastrointestinal system 59
6 The digestive system (liver, biliary tract and
pancreas) 93
7 The urinary system 117
8 The central and peripheral nervous system 137
9 The skeletal system 171
10 The skin 185
11 The endocrine-hormonal system 195
12 The nutritional system and acid-base balance 215
13 The blood and lymphatic system 241
14 The psychological system 265
15 The common infections 281
Index 295
5
List of Differential Diagnosis Tables
Central chest pain 34

~~ m
Difficulty in breathing: dyspnoea 52
Chest pain on breathing 54
Vomiting due to gastrointestinal disorders 84
Diarrhoea - 1 86
Diarrhoea - 2 88
Abdominal pain due to gastrointestinal disorders 108
Ascites due to hepatic diseases 112
Pain on urination 128
Haematuria 130
Oliguria and anuria 134
Loss of consciousness 166
Joint pains 180
Skin rashes 190
Specific endocrine problems 212
Vitamin deficiency 236
Electrolyte and acid-base disturbance 238
Anaemia 260
Anxiety and depression 276
Common infections 290
6
Foreword
This book is designed for use by medical students, nurses,

young practitioners, internists, family physicians and all those
initially involved with the problem of diagnostics. It is struc-
tured to provide a concise logical approach to the diagnosis of
common illness and disorders in adults. The elucidation of an
illness cause is not easy for the inexperienced. Although text-
books and guidance notes can be referred to for clarification of
assembled thought - once a medical history has been taken - a
system-orientated reference guide has considerable value for
aiding and checking the logic of diagnosis.
It is hoped that this book will fulfil that purpose. It could not
have been written without the help of R. G. Brackenridge's
Essential Medicine (1979, MTP, Lancaster, England), and
J. Fry's Common Diseases (1979, MTP, Lancaster, England),
to which the reader is referred and to which generous acknow-
ledgement is made. The tables of Differential Diagnosis that
follow Chapters 3-7 are adapted from some that have
appeared in Handbook of Differential Diagnosis, vols 1-3,
published by Rocom Press, Hoffman La Roche Inc., New
Jersey, 1968-1974 - an invaluable publication now unfortun-
ately out of print, and permission to do so is gratefully apprec-
7
8 DIFFERENTIAL DIAGNOSIS
iated. Finally without the stimulus and encouragement of

Mr David Bloomer (MTP) and the particular assistance of
Mrs J. C. Robinson, this book would never have been written.
ALEXANDER D. G. GUNN
Reading, Berks, UK
1981
Chapter 1
Introduction - How to Use
this Book for Reference
A guide to differential diagnosis, unless it ran to several

volumes, could never encompass all aspects of every known
form of disorder or disease. The common disorders and ill-
nesses, however, wherever they are met, share the specific
characteristics of common symptoms and signs that can be
elicited in taking the patient's history and in the physical
examination that follows. In general an illness will affect one
or other of the patient's major physical systems and this book
provides reference systematically to the common disorders and
illnesses - by listing the symptoms and signs and describing the
routine diagnostic investigations. As a revision course in
preparing for examinations, the major differential aspects of
diagnoses are listed in the text and tabled at the end of the
relevant chapters. As a guide to the key laboratory investig-
ations in diagnosis, the chapters and the tables detail the
routines that would apply in confirming the suspicion formed
by examination of the patient. No book, however, will ever
replace the wisdom gained by experience in the practice of
medicine and all practitioners will need to constantly update
their knowledge of medical science by continued reading of the
9
relevant literature. This book, therefore, is a guide, logically

presenting information about illness and disorder that enables
the doctors or students of medicine and nursing newly in
practice to check and constantly improve their diagnostic
ability.
When a patient's history has been taken, the first step in the
clinical reasoning process is to decide which of the findings
that have been elicited are relevant to the discovery of the
possible disease. The initial symptoms are those which are
presented by way of verbal communication; other symptoms
are elicited and the signs of disorder are detected by the
physical examination - but this has to be done in a routine
manner in order to ask the specific cross-checking questions.
Differential diagnosis is essentially a process of logical thought
- not dissimilar from a mental flow chart as written for
computer programming. Focusing on a system disorder
enables the clinician to consider all the likely possible causes
and to reflect on the necessary laboratory tests for ultimate
confirmation. Sixty per cent of the diagnosis is made at the
history-taking stage in the experienced - since the practice of
medicine is essentially that of problem analysis. The patient
presents with the problem, the clinician has to know, or define,
its common causes, be aware of its more probable cause in that
specific patient, and to ascertain through examination and
laboratory testing the specific cause for that particular patient
- in order to provide any form of therapeutic advice or
management. It is a process of systematically testing hypo-
theses.
The first hypothesis, therefore, is the patient claiming that
there is a system disorder. Each chapter of this book opens
with a brief survey of the frequency of such system illnesses
and their broadest epidemiological pattern. The diagnoses of
common disorders, however, depend on certain particular
types or forms of clinical investigation - be it blood test, urine
examination, X-ray etc., and these are listed to act as an aide
memoire for the clinician. The common relevant symptoms are
then listed, to be followed by further discussion of the appro-
priate tests. Thus, before reaching the text detailing the
disorders themselves, the reader is primed with the basis of
problem-solving knowledge. The common disorders and
INTRODUCTION 11
diseases are then described and detailed, with causes and the
specific symptoms and signs listed. Recommendations with
regard to further investigations are made where appropriate.
The pattern of the text, therefore, is that of initial broad
consideration of the diseases, epidemiologically, followed by
clinical and diagnostic detail.
Chapter 2
The Medical History
Taking a medical history is a skill, acquired by most as a result

of experience and taught to the student as the very basis of all
diagnostic accuracy. It is an interview that should be struc-
tured between patient and clinician and from it has to emerge:
(1) the reason the patient sought help,
(2) the circumstances and details of the illness,
(3) the previous medical history,
(4) a family history,
(5) an occupational history,
(6) medication taken, and current or previous attempts to
modify or treat the symptoms,
(7) social drug usage (tobacco, alcohol or others),
(8) an assessment of the function of the main body systems.
Whilst the interview is taking place, the clinician will be form-
ing a further assessment of two important factors relevant to
the diagnosis:
(1) the severity of the complaint,
(2) its relevance to that individual's life pattern.
13
There are, however, only two questions that require answering

with regard to the problem posed:
What is its cause?
What are its consequences?
In these two questions lie the whole direction of the clinician's
subsequent activity, for they determine the process of the
routine physical examination, the laboratory investigations,
the confirmation of the diagnosis and the ultimate treatment
and follow-up. Thus diagnosis is essentially the answering of
these questions.
At the history-taking stage, these questions will be in the
mind of the clinician from the very beginning - they are
implicit even if the patient is unconscious and unable to
verbally communicate at all. In the routine of the standard
medical interview, however, they are constantly guiding the
interrogative remarks and direction of both conversations.
Although the patient cannot necessarily present the inform-
ation to the doctor in the ideal logical form that answers them
- the patient actually has the same questions in mind, and has
had ever since a disturbance of function has been noticed.
There is thus - except in the mentally disordered, pre-
comatose, or very ill- an implicit agreement that the medical
history-taking is leading to the answers being produced. Co-
operation, therefore, is usual; the difference in the relationship
is that the doctor guides the conversation.
Verbal communication is, however, liable in all circum-
stances to be fraught with distraction, digression, misunder-
standing, or failure in comprehension - on the part of both
participants - that is why in medicine it has to be a mental
discipline. Computer diagnosis, by means of question and
answer through a visual display unit's keyboard, can never
replace the empathy, voice tonality or demeanour recognition
that can be conveyed only by human contact. Factual histories
may be more rapidly, or in some cases, conveniently elicited
but diagnostic histories are not always, or even simply, a
matter of fact, they require impressions to be formed, attitudes
to be assessed and important emphases to be recognized that
cannot be conveyed by specific Yes-No answers.
A medical history is 'taken' from a patient, not given,
THE MEDICAL HISTORY 15
offered or simply produced - it is a process of extraction and
distillation. That is why each chapter that follows emphasizes
repetitively that any diagnosis of disorder will depend on
symptoms, history, observation of the patient and examin-
ation of a routine series of recommendations. For the history-
taking is an inseparable part of the observation of the patient
and in it lies the art of medical practice - the science is in the
confirmation of the diagnosis.
Chapter 3
The Cardiovascular System
The commonest disorders of the cardiovascular system are

hypertension, coronary artery disease, varicose veins, heart
failure, and cardiac arrhythmias, phlebitis and peripheral
artery disease in that order of frequency. Death will be caused
most frequently through coronary artery disease and 51070 of
all deaths in Britain and the USA are from circulatory disease.
Disorder of the cardiovascular system is predominantly a
result of age.
Diagnosis of disorder will depend on symptoms, history,

observation of the patient and examination of:
(A) pulse,
(B) blood pressure,
(C) heart sounds (auscultation),
(D) electrical tracing of the heart muscle activity (electro-
cardiogram).
(A chest X-ray and serum electrolyte measurements with other
blood tests will also be necessary)
17
Common symptoms of generalized disorder will be:

(1) breathlessness (on exertion or lying flat),
(2) cyanosis (blue discoloration of face, lips and fingertips),
(3) oedema (ankle swelling),
(4) chest pain,
(5) headaches,
(6) palpitations,
(7) confusion or restlessness,
(8) loss of consciousness.
(A) EXAMINATION OF THE PULSE

Consider the rate, rhythm and force of the pulse. The normal
rate is 60-80 per minute.
RATE
A rapid pulse, tachycardia, can result from increased metabol-
ism (exercise, emotion, fevers, thyrotoxicosis), blood loss, and
cardiac disorders.
A slow pulse, bradycardia, occurs in simple faint (syncope,
vasovagal attack), heart block, and digoxin overdosage.
RHYTHM
Irregularity occurs in:
Sinus arrhythmia - normal in youth, the pulse rate increases
with inspiration, and decreases on expiration.
Paroxysmal tachycardia - sudden burst of regular beating,
rate 150-200; not usually a sign of heart disease, but heart
failure may occur if the attack is prolonged.
Atrialfibrillation - due to:
(1) rheumatic heart disease involving the mitral valve,
(2) ischaemic (coronary) heart disease,
(3) thyrotoxicosis.
The atria are twitching rapidly and irregularly at around

30Q-4oo 'beats' per minute. The conducting bundle cannot
THE CARDIOVASCULAR SYSTEM 19
respond to such a high rate, and the ventricles beat at an
irregular 100-200 per minute.
A trial flutter - this is relatively rare and may be caused by the
same heart diseases as atrial fibrillation. The atrium is 'flutter-
ing' at a regular 200-400 beats per minute, again there is a
block (which may be variable) in the conducting tissues, and
the ventricular rate is less than 150, generally regular.
Extrasystoles (ectopic beats) - these arise from an abnormal
focus in the atria (supraventricular extra systoles) or in the
ventricles. They may be unimportant, with no associated heart
disease, or important in digoxin poisoning (coupled beats) and
after myocardial infarction.
Heart block - due to some or all of the stimuli from the atrial
pacemaker failing to reach the ventricular muscle. Thus the
block may be incomplete with missed beats and irregular
rhythm, or complete when the ventricle takes up its own
rhythm at a regular 40 beats per minute or less. Heart block
may occur in myocardial infarction.
(B) EXAMINATION OF THE BLOOD PRESSURE

The blood pressure is measured with the sphygmomanometer.
The cuff is applied to the upper arm, inflated until the mercury
is above the level where the pulse is no longer palpable, then
deflated while one listens with the stethoscope over the
brachial artery. The level at which pulse sounds become
audible is called the systolic blood pressure. As the cuff is
deflated further, the sounds become faint and then inaudible.
This is the diastolic reading. The systolic pressure depends on
the force of the cardiac contraction and the state of the walls of
the large vessels, being higher in the elderly whose vessels are
harder and less elastic than those in young people. The
diastolic pressure corresponds to the resting pressure in the
artery between heart beats. The intensity of the blood pressure
sounds may be diminished if the cardiac output is poor, when it
may be difficult to be sure of the systolic and diastolic
readings, and it is not always possible to record within 2 mm. A
fat arm causes a falsely high reading. The normal blood

pressure is:
100-140 (systolic)
70-90 (diastolic)
A falling blood pressure indicates haemorrhage or deteriorat-

ing cardiac function, but cardiac disease may exist with a
normal blood pressure.
(C) EXAMINATION OF THE HEART SOUNDS

The heart is a muscular pump with four chambers - the right
atrium, which receives venous blood from the systemic veins;
the right ventricle, which pumps the blood through the
pulmonary artery to the lungs to be oxygenated; the left
atrium, which receives this blood from the lungs; and the left
ventricle, which pumps blood through the aorta to reach
arteries and capillaries throughout the body.
At each beat the ventricles contract simultaneously to expel
their blood, the heart valves (tricuspid and pulmonary on the
right side, mitral and aortic valves on the left) preventing
backward flow. The heart beat causes a wave palpable as the
pulse in a peripheral artery. The heart sounds, audible with the
stethoscope over the 'apex' medial to the left nipple, are two in
number, 'lup-dup'. They are due to the valves closing at the
beginning and end of the contraction phase, which is called
systole, and this is followed by the resting and filling phase, or
diastole.
(D) ELECTROCARDIOGRAM
Cardiac contraction is 'fired' by an electrical stimulus, arising
at the pacemaker in the sinoatrial node, spreading through the
right atrium to reach the atrioventricular node, then down an
electrical 'bundle' between the ventricles; this bundle divides
into two branches and the stimulus thence passes out into the
ventricular muscle (myocardium). This tiny electric current
can be detected by applying plates or 'electrodes' to the chest
and limbs, and recorded on paper or displayed on an oscillo-
scope (monitor) - the electrocardiogram (ECG).
Disturbances of rate and rhythm may arise anywhere in the
electrical conducting system. While they may be detectable by
feeling the pulse or by listening to the heart, an ECG is essential
for accurate diagnosis and treatment.
p T
The P wave denotes atrial activity, the QRS complex and the
T wave ventricular activity.
Common Disorders of the Cardiovascular

System
(1) HYPERTENSION (HIGH BLOOD PRESSURE)
The normal blood pressure ranges from 120/80 for a person in
his twenties to about 160/90 in his sixties. The diastolic level is
raised from narrowing of small arteries and arterioles. A raised
diastolic pressure is usually accompanied by a raised systolic
pressure. The effects of hypertension on the heart, kidneys and
retinae of the eyes are more important than arbitrary blood
pressure readings, which may be influenced by emotion. The
finding of a raised blood pressure in a symptomless patient
should direct attention to these organs, and treatment will
prevent further damage to them.
Rare causes
Coarctation of the aorta - a congenital narrowing of the aorta
just beyond its origin at the heart; occurs in the young; radial
pulses normal, but femoral pulses diminished or absent.
Adrenal gland causes.
Tumour of medulla, producing adrenaline-like substances

excreted in the urine, causes hypertension, often paroxysmal,
accompanied by sweating.
Over-activity of adrenal cortex, producing trunk obesity and
skin 'staining' from excess cortisol production, measurable in
the urine.
Tumour of adrenal cortex, producing polyuria, weakness and
low serum potassium.
Common causes
Renal disease: chronic glomerulonephritis,
chronic pyelonephritis,
renal artery stenosis.
These may cause the kidney to produce renin, a substance
which raises the blood pressure, and which also stimulates the
adrenals to produce aldosterone, further raising the blood
pressure.
Toxaemia of pregnancy - placental hormones may playa part,
and there is accompanying albuminuria and oedema, and fits
(eclampsia) in severe cases.
No definite cause can be found in the vast majority of cases,
when the term essential hypertension is used. There may be a
family history, suggesting a hereditary basis in some cases.
Symptoms and signs

The finding of a raised blood pressure is common, especially in
women after the menopause; the condition may be symptom-
less and in the elderly it is often harmless. The symptoms and
signs of hypertension are in fact due to its effects on the heart
and blood vessels, especially the cerebral arteries and smaller
vessels in the retina of the eye, and effects on the kidneys.
Headache is not a common complaint except in severe hyper-

tension.
Epistaxis (nose bleeding) may be a mode of presentation.
Breathlessness. The left ventricle must pump against the
increased pressure in the arteries, gradually enlarges, shows
signs of strain detectable on ECG and eventually fails; the
resultant pulmonary oedema causes breathlessness on
exertion, and on lying flat in bed nocturnal dyspnoea.
Pre-existing coronary artery disease may be made worse.
Cerebral haemorrhage. Arteriosclerotic disease affecting the
internal carotid artery and the intracerebral vessels is worsened
and a vessel may break down causing cerebral haemorrhage
(and often death); there is also an increased risk of cerebral
thrombosis. The smaller intracranial arteries may be affected
causing cerebral oedema, and the condition of hypertensive
encephalopathy, with headaches, fits, disturbance of con-
sciousness and transient episodes of paralysis.
Visual disturbance. The retinal arteries may be affected and
severe cases have visual upset and retinal haemorrhages and
papilloedema (blurring of the optic discs) - visible with the
opthalmoscope.
Polyuria. Not only may kidney disease cause hypertension, but
hypertension from any cause will in turn damage the kidneys.
The renal units (nephrons) are gradually destroyed, and
remaining nephrons work at maximum level, but the kidneys
are no longer able to reproduce concentrated urine. They can
only eliminate the body's waste products, such as urea, in large
quantities of dilute urine (polyuria). The patient may admit to
having to rise at night to pass urine, and may complain of
thirst. The blood urea gradually rises, and if the condition is
untreated, the patient passes into renal failure with dehydra-
tion, vomiting, coma and death.
These effects of hypertension may be very gradual, with pro-

gressive deterioration over many years. In some younger
patients, however, the process is much more rapid, and is
called malignant or accelerated hypertension - with very high
diastolic pressure (over 140 mmHg), retinal haemorrhages and
papilloedema, and progressive renal failure.
Investigations in hypertension
(1) Charting of the blood pressure.
(2) Urine: specific gravity - fixed at 10.10 with renal involve-
ment, may contain albumin; laboratory examination

may show red cells and casts, and superadded renal infec-
tion causes pus cells and positive bacteriological culture
(colony count); 24-hour specimens sent for corticosteroid
assay (in suspected Cushing's syndrome).
(3) ECG - shows left ventricular enlargement or strain.
(4) Chest X-ray - shows enlarged heart, and early pulmonary
oedema.
(5) Intravenous pyelogram X-ray (IVP) - assesses size and
function of kidneys.
(6) Serum 'electrolytes' (sodium and potassium) and the
blood urea level.
(2) CORONARY ARTERY DISEASE

Coronary heart disease is the commonest single cause of death
amongst middle-aged men.
The heart muscle receives its blood supply from the coron-
ary arteries, and these are affected with ageing, by the process
of arteriosclerosis. Plaques of fatty material are laid down in
the arterial lining (atheroma); calcium may be deposited in the
plaques. Minute clots (thrombi) tend to form on the irregular
surface, further narrowing the lumen (bore) of the artery so
that the heart receives insufficient blood for its own needs.
Causes
High animal fat intake has been blamed, and also a diet too
rich in refined carbohydrate and sugar. Arteriosclerosis is less
common in races with a more natural diet including bran and
fibre, and in those taking polyunsaturated oils rather than
animal fats. A disturbance of the blood clotting mechanism
has also been postulated.
Coronary heart disease is much commoner in men, but women
who take oestrogen-containing contraceptive pills are at
increased risk.
There is a definite association with heavy cigarette-smoking.
Lack of exercise may also playa part. The stress and strains of
modern life may have some effect as adrenaline release affects
the blood fats. Raised blood pressure and obesity aggravate
the condition.
Symptoms and signs
Angina pectoris
The blood supply through the narrowed coronaries is
inadequate during effort; the impaired metabolism results in
the formation of substances that cause pain.
There is a constricting central chest pain brought on by
exercise, especially hill-climbing, or emotional excitement,
and relieved by rest. The pain may radiate to the arms,
especially the left arm, and the lower jaw. The patient may
describe the tight feeling as one of difficulty in getting his
breath. There are no consistent pulse or blood pressure
changes, but patients generally have an abnormal ECG.
Myocardial infarction (heart attack)

This is due to a sudden blockage of a narrowed artery by clot,
hence the term coronary thrombosis.
A part of the heart's blood supply is suddenly cut off, causing
'infarction' which means death of an area of tissue. If a vital
part of the electrical conducting tissue is involved, even a small
infarct may cause arrhythmia and sudden death from cardiac
arrest (see below) yet the rest of the heart muscle may be
undamaged. The infarct goes through processes of healing
similar to those in a wound, scar tissue ultimately replacing the
damaged area of myocardium.
There is chest pain, similar in site and distribution to angina,
but more severe and prolonged, and not necessarily related to
exertion - symptoms may arise when the patient is in bed.
Severe pain is accompanied by sweating, nausea and vomiting,
and by restlessness. There may be a feeling of extreme breath-
lessness and of impending doom.
Severe cases have pallor, cyanosis with cold extremities,
irregularities of the pulse (which may be rapid or slow) hypo-
tension, and rapidly developing pulmonary oedema and con-
gestive heart failure.
Cardiac arrest
Cardiac arrest is due to ventricular fibrillation (the ventricular
muscle twitching but failing to give a proper contraction) or to
all its movements ceasing. In both cases there is a sudden

failure of the circulation, and the brain can survive for only
3-4 min. It may have occurred through:
(1) myocardial infarction;
(2) pulmonary embolism, when the pulmonary circulation is
blocked by clots from the veins;
(3) severe haemorrhage;
(4) electrocution and drowning.
There is sudden collapse, loss of consciousness, absence of
pulse and of heart beat, increasing cyanosis often with gasping
respiratory efforts; pupils become dilated and patient will die
if left untreated.
Summon help - alarm call in hospital.
Lay patient flat on a firm surface (bed boards or the floor) but
elevate the legs.
Give a sharp thump on the patient's chest - this may restart the
heart. If not, proceed with external cardiac massage - apply
the heel of one hand to the lower sternum and with the other
hand on top compress the sternum backwards some 3-4 cm
about 80 times per minute.
Artificial ventilation - remove false teeth, clear the airway by
supporting the chin well forward, insert airway if available.
Inflate the lungs by mouth-to-mouth breathing once for every
five chest compressions.
Investigations in coronary artery diseases
(1) charting of blood pressure and pulse rate;
(2) charting of urine output;
(3) ECG and continual ECG monitoring;
(4) blood level assessment of cardiac muscle enzymes (SGOT
and SLDH) and serum electrolytes;
(5) white cell count and ESR;
(6) chest X-ray- coronary angiogram (only in cases going on
for cardiac surgery).
(3) HEART FAILURE
This may occur acutely, after massive myocardial infarction,

or can be a gradual process over months or years. Often the
heart muscle has enlarged despite ischaemia, or in the attempt
to maintain cardiac output with diseased valves, but ultimately
the myocardium fails.
Thus heart failure is pump failure. It is associated with salt
and water retention, related to impaired circulation to the
kidneys. Salt retention causes water retention, and the result is
an excessive blood volume, so that the circulation becomes
overloaded, further embarrassing the heart.
Causes
Left ventricular failure results from ischaemic, hypertensive,
and aortic or mitral valve disease, for in these conditions the
brunt of the trouble is borne by the left ventricle. Symptoms
result from back-pressure on the vessels in the lungs, causing
pulmonary oedema.
Right ventricular failure follows left ventricular failure, but
may occur first in some cases of mitral stenosis where there is
constriction of the blood vessels in the lung producing right
ventricular strain.
Chronic bronchitis and emphysema also throw a strain on the
right side of the heart.
Right ventricular failure results in systemic congestion - raised
venous pressure, swollen liver and peripheral oedema.
Precipitating factors: in patients with known heart disease,
heart failure may be precipitated by a further myocardial
infarction or an episode of arrhythmia.
Intercurrent infection, especially respiratory infection, and
anaemia are non-cardiac precipitating factors.
Symptoms and signs

Breathlessness - (dyspnoea, difficulty in breathing) may be
noted first on exertion or stair-climbing. In left ventricular
failure and pulmonary oedema, breathlessness when the
patient is woken from sleep is characteristic. This occurs from
increased lung congestion when the patient lies flat, and is
relieved by sitting up in bed. In heart failure generally, patients
feel less dyspnoeic when propped up. Severe pulmonary
oedema causes extreme breathlessness and the production of

frothy red sputum.
Cyanosis - blue discoloration of lips, cheeks and fingertips
from sluggish peripheral circulation and reduced oxygen
content of the blood in the capillaries. The skin is usually cold,
except in heart failure following pulmonary disease, when the
extremities may be warm.
Oedema - fluid retention in tissues and in heart failure is
gravitational; thus there is oedema (pitting with finger
pressure) over the ankles and legs, or above the sacrum if the
patient has been confined to bed. Swelling of the abdomen
may be due to ascites, fluid exudation into the peritoneal
cavity. In right heart failure the jugular venous pressure is
raised and pulsation is visible in the neck. The liver may be
tender and swollen.
Restlessness and confusion - due to cerebral anoxia; there may
be Cheyne-Stokes breathing from affection of the respiratory
centre in the brain. This is a form of periodic breathing -
depression of the respiratory centre causes apnoea (no
breathing) followed by carbon dioxide retention which
stimulates the centre into causing deep sighing respirations.
Pulse rate - usually raised, and may be regular or irregular.
The commonest irregularity is atrial fibrillation with a rapid
ventricular rate. Not all the beats of the heart may be strong
enough to reach the periphery so that the apical rate may be
higher than the pulse rate - pulse deficit.
Blood pressure - may be normal, raised (e.g. in hypertensive
failure) or low; a low blood pressure associated with cold, blue
extremities indicates poor cardiac output and carries a bad
prognosis.
Lack of appetite, nausea and vomiting - occur from conges-

tion of the stomach, and impaired circulation to the large
bowel causes constipation or occasionally diarrhoea.
Urinary output - may be lowered from poor circulation to the

kidneys, and there may be albuminuria. Electrolyte disturb-
ances (sodium and potassium) are part of the picture of cardiac
failure. Not only is there sodium and water retention, but there
is also potassium loss rendering the heart more irritable and
liable to arrhythmias.
Venous thrombosis - in the legs, with risk of pulmonary
embolism, may occur from circulatory slowing, and is an
important complication of cardiac failure.
(4) PERICARDITI S
Pericarditis is inflammation of the pericardial sac covering the
heart. Pericarditis may be 'dry', or there may be a pericardial
effusion.
Causes
As a complication of rheumatic fever (part of the 'carditis' of
severe cases), or of myocardial infarction, and in the late stages
of renal failure.
Acute viral infection.
Rheumatoid arthritis and collagen diseases.
Myxoedema.
Spread of infection from lung or pleura.
Symptoms and signs

In rheumatic fever and myocardial infarction the symptoms
are mainly those of the underlying condition, with more super-
ficial chest pain and a pericardial 'friction rub' heard with the
stethoscope.
In young adults, where Coxsackie virus infection may be a
cause, associated symptoms such as cough, sore throat and
muscular pain are present.
There is fever and retrosternal pain.
There is a friction rub and typical ECO changes of pericarditis,
but the myocardium is not involved to any extent and the
cardiac enzymes (SOOT and SLDH) are not raised.
Pericarditis with effusion - these prevent the proper pumping
action of the heart, especially the right ventricle, causing right
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Electrocardiogram showing ST segment shifts

appropriate to acute pericarditis
ventricular failure - distended neck veins, enlarged liver and

peripheral oedema. These signs are out of proportion to
breathlessness, and the patient may lie flat without dyspnoea
as the lungs are not engorged.
There may be a complaint of weakness from poor cardiac
output, with small pulse and low blood pressure.
In pericardial effusion the cardiac shadow on X-ray is
enlarged.
Ultrasonic scanning may show fluid levels present.
(5) PULMONARY EMBOLISM

Causes
Arises from deep vein thrombosis in the leg.
Venous thrombosis is a complication of bed rest, especially in
those with cardiac failure.
Obesity.
Following abdominal operations.
In those on the contraceptive 'pill'.
Symptoms and signs
In about half the cases there is evidence of leg vein thrombosis
such as calf pain and oedema, but often the clot has arisen
silently from upper parts of the vein in the thigh, and the first
sign of trouble is in the lungs or heart:
Pulmonary infarction - pain on breathing, from pleural

involvement.
Breathlessness.
Haemoptysis (blood in the sputum).
Rise in pulse rate.
A pleural rub may be heard with the stethoscope, and there
may be X-ray changes.
Massive pulmonary embolus - a large clot may completely

obstruct the pulmonary artery, with sudden collapse.
Severe breathlessness.
Cyanosis.
Chest pain.
Raised jugular venous pressure.
Rapid thready pulse with low or immeasurable blood pressure.
Death will follow unless the clot breaks up or can be speedily
removed surgically.
(Special investigations include pulmonary angiography and
lung scanning with radioactive isotopes, but there may be no
time for these in severe cases.)
(6) PERIPHERAL ARTERIAL AND VASCULAR DISEASE

The victims again are middle-aged men, and the elderly of both
sexes. Cigarette-smoking and obesity are predisposing factors,
and arteriosclerosis of the distal leg arteries, and those in the
feet, is commoner in diabetics.
CHRONIC ARTERIOSCLEROSIS OF
LOWER LIMB VESSELS
Cause
Arteriosclerotic narrowing and varying degrees of obstruc-
tion, involving the iliac arteries in the pelvis, and femoral
vessels (and their branches) in the thigh. The condition may
spread to involve distant arteries, but in diabetics vessels in the
feet may be involved before there is gross disease.
Symptoms and signs

Intermittent claudication. The patient may complain that his
pulses are impalpable, the leg loses its hairs, the skin is pale and
may have a shiny appearance and is cool to the touch.
Wounds heal poorly and are liable to infection.
Severe cases develop 'rest pain,' occurring characteristically
during the night, the patient putting his feet on a cold floor in
an attempt to gain relief. This indicates extensive disease, with
risk of skin breakdown and gangrene.
Investigations
Investigations should be made for conditions such as heart
failure.
Anaemia.
Diabetes.
In younger patients in whom there is no evidence of
generalized arterial disease, arteriography should be carried
out to ascertain if there is a localized segment of arterial
narrowing amenable to surgery.
ACUTE ARTERIAL OBSTRUCTION

Cause
This is usually an embolus from the left side of the heart, from
thrombus in the left atrium in mitral stenosis, or from
thrombus under a myocardial infarction. Clot may also
become detached from a large arteriosclerotic vessel, or form
over an existing arteriosclerotic plaque.
Symptoms and signs
Sudden severe pain.
Pallor (or cyanosis from associated venospasm).
Coldness.
Loss of sensation and muscular weakness in the affected limb.
Absent arterial pulses. Patients usually have a history of
arterial disease, or may be in heart failure, but the condition
may occur without previous symptoms.
RA YNAUD'S SYNDROME
This is due to spasm of the small arteries of the fingers and
hands. It is commonest in young women, who complain of
pallor and numbness of the fingers on exposure to cold.
Similar symptoms may occur in men using vibrating tools,
and in autoimmune disorders such as scleroderma, where
destruction of the small vessels, and gangrene, may follow.
VENOUS THROMBOSIS AND EMBOLISM

Deep vein thrombosis
This is the presence of thrombus (clot) in the deep veins of the
calf, but the femoral vein in the thigh may also be involved.
Causes
Bed rest, especially if circulatory slowing occurs as in conges-
tive cardiac failure.
Surgical operations; thrombus often develops at the time of
operation, but spreads in the following days due to alterations
in the coagulability of the blood.
Pregnancy, and contraceptive tablets of high oestrogen
content. Neoplasm, often hidden, e.g., carcinoma of
pancreas.
DIFFERENTIAL DIAGNOSIS OF CENTRAL CHEST PAIN

Character Location Radiation Duration
Angina pressing substernal shoulders, usually

pectoris crushing, arms, neck, 1-3
bursting jaw min
Coronary pressing, substernal shoulders, few

insufficiency crushing, arms, neck, minutes
bursting jaw to several
hours
Myocardial pressing substernal shoulders, less than

infarction crushing, arms, neck, an hour to
bursting jaw several days
Acute crushing or substernal shoulders, days to

pericarditis sharp neck, or back weeks
(not arms or
jaws)
Pulmonary sudden and substernal chest, minutes

embolus oppressive shoulders, to hours;
epigastrium may recur
Onset Associated signs EeG changes

and symptoms
exertion; fear and anxiety; ECO may show ST

emotional patient pale, sometimes depression during
stress sweating; may have exercise
apical presystolic gallop
rhythm to heart sounds
usually at fear and anxiety; ECO may show ST and T

rest dyspnoea; patient pale changes; temperature
and often sweating; normal; SOOT elevation
may have fast pulse may be detected within
rate first 7-14 days if infarct
develops
usually at fear and anxiety; Q waves and other

rest dyspnoea; weakness; acute changes on ECO;
shock; arrhythmia; SOOT and temperature
acute left ventricular elevated
failure
usually at fever; non-productive ST elevation and T

rest cough; pericardial inversion in bipolar limb
friction rub; paradoxical and precordial leads
pulse in more severe
usually at marked dyspnoea; rapid shift of QRS axis to

rest shallow breathing, often right bundle branch
cyanotic; low blood block
pressure; haemoptysis
and pleural pain later
Symptoms and signs

Calf pain and tenderness.
Ankle oedema.
Sometimes slight rise of temperature.
Investigations
Include the use of ultrasound with the portable Sonicaid
detector, which fails to emit its characteristic flow-noise if the
circulation is obstructed.
Injected radioactive fibrinogen may be detected at the site of
thrombosis by using a special counter.
X-ray venography may be necessary to localize the site and
extent accurately.
Superficial vein thrombosis (phlebitis)

Thrombosis in a superficial vein may occur after injury or use
of indwelling cannulae for intravenous infusions. The
condition may occur spontaneously in the legs, especially in
relation to varicose veins.
Symptoms and signs

Local pain.
A red tender area along the line of the vein, which may be
palpable as a thrombus-containing cord.
Chapter 4
The Respiratory System
Respiratory diseases are the most common cause of illness, at

all ages, but account for a relatively small proportion of all
hospital admissions. Acute respiratory infections and asthma
are the most frequent cause of hospitalization in the younger
patient, with chronic bronchitis, cancer of the lung and
broncho-pneumonia in the older. Twenty per cent of all deaths
in Britain and the USA are from respiratory disease, but with
advancing age it is from pneumonia, chronic chest disease and
lung cancer in that order of frequency.
Diagnosis of disorder will depend on symptoms, history of the

patient and examination of:
(A) respiration rate and character,

(B) chest sounds (auscultation),
(C) chest X-ray,
(D) sputum,
(E) peak expiratory flow rate,
(F) blood gas analysis.
37
Common symptoms of respiratory disease will be:

(1) cough,
(2) dyspnoea (breathlessness),
(3) sputum production (and/or haemoptysis),
(4) chest pain,
(5) cyanosis (blue discoloration of face, lips and fingertips),
(6) clubbing of the fingertips.
(A) RESPIRATION RATE AND CHARACTER

Control of respiratory movements is maintained by a centre in
the medulla of the brain. It is sensitive to carbon dioxide in the
blood, excess of which stimulates respiration and to the blood
oxygen level, lack of which (anoxia) further stimulates the
breathing rate. A rapid rate is thus brought about by the
demands of exercise, an alteration in blood gas levels, an
increase in the metabolic rate (as in any generalized infection
and fever) and generalized disease or disorder of the respir-
atory system. Dyspnoea means difficult breathing, an
unpleasant awareness of the act of breathing. It is usually due
to oxygen-lack, thus in acute respiratory disease such as
pneumonia there may be rapid shallow breathing.
In chronic bronchitis and emphysema the mechanics of
respiration, the bellows function of the lungs, has suffered and
the patient is dyspnoeic and distressed. His rib cage lifts
instead of expanding properly, and his respiratory efforts
involve the use of the neck muscles rather than the diaphragm.
In lung fibrosis the patient is breathless on slight exertion,
but not necessarily dyspnoeic at rest.
Dyspnoea may be due to the pain of pleurisy, the patient
being afraid to take a deep breath.
Wheezing due to bronchospasm accompanies the breathless-
ness of asthma, and the patient has special difficulty in
expiration.
Stridor is noisy inspiration from inflammation or obstruction
of the larynx, trachea or large bronchi.
Periodic breathing or Cheyne-Stokes breathing is where a
period of apnoea (no breathing) occurs, then, as carbon diox-
THE RESPIRATORY SYSTEM 39
ide builds up in the blood, stimulation of the respiratory centre
occurs and deep sighing respirations develop, followed again
by apnoea.
Air hunger is continuous deep breathing due to stimulation of
the respiratory centre by acidosis.
(8) CHEST SOUNDS (AUSCULTATION)

Through a stethoscope the characteristic sounds of wheezing
or stridor, as above, are magnified, but over local areas of the
chest crepitations can be heard where the bronchial passages
and the lung tissue is inflamed (as in bronchitis or
pneumonia). A pleural rub may be detected in pleurisy, or
areas of the chest where all respiratory sounds are diminished
when there is lung or lobar collapse in pneumonia or pneumo-
thorax. A knowledge of the normal anatomy of the thorax is
necessary to compare breath sounds side by side.
(C) CHEST X-RAY

This is an essential addition to clinical examination of the
chest. A portable film may be taken in the ward if the patient is
too ill to move to the X-ray department.
A tomogram is a special view focused on the lesion.
A bronchogram is an X-ray following injection of radio-
opaque iodized oil through the mouth or larynx to outline the
bronchi.
(D) SPUTUM EXAMINATION

Purulent sputum denotes infection.
Bacteriology (staining and culture), reports should be con-
sidered in the light of the clinical findings, and response to
treatment.
A knowledge of the infecting organism and its sensitivity
allows adjustment of treatment if necessary.
Cytology for malignant cells is possible in suspicious cases and
especially useful if the sputum is blood-stained.
(E) PEAK EXPIRATORY FLOW RATE

This is measured by rapid exhalation into a peak flow meter - it
indicates the 'bellows' efficiency of the lungs and is impaired in
airways obstruction, chronic bronchitis, and asthma.
The normal rate is 500 litres per minute.
(F) BLOOD GAS ANALYSIS

Arterial blood specimens are examined for their oxygen and
carbon dioxide content, expressed as Pa 2 and Pco 2 respec-
tively. The effect of changes in these on the acidity of the blood
is measured as the pH.
(Further special investigations would include laryngoscopy,
bronchoscopy, spirometry and ventilation perfusion tests).
Common Disorders of the Respiratory

System
(1) INFLUENZA
Cause
The influenza viruses. These have recently spread in epidemics
from the Far East. Thus influenza virus A2, Hong Kong strain,
caused epidemics in Britain in 1968 and 1970. The diagnosis is
relatively easy during recognized epidemics. In non-epidemic
years, the term 'influenza' is often vaguely applied to any
febrile illness of uncertain cause.
Symptoms and signs

Fever.
Headache.
Cough.
Sore throat and catarrh.
Often of sudden onset and associated with limb pains and
prostration.
Influenza-like illness, not necessarily due to the same virus,
may be associated with conjunctivitis and running eyes, and
sore throat.
Complications
Complications include bronchitis and pneumonia; these are a
serious hazard in those with existing respiratory disease.
(2) DISORDERS OF THE LARYNX

Acute laryngitis may complicate a cold or respiratory infec-
tion, and present hoarseness, with cough and sputum.
Croup in children is due to laryngo-tracheo-bronchitis, caused
by a virus, but superadded bacterial infection may seriously
aggravate the disorder.
Angioneurotic oedema, an allergic reaction to something
inhaled, ingested, or injected, may be so severe as to cause
laryngeal oedema and obstruction.
Chronic laryngitis occurs in auctioneers and those who over-
use the voice, especially if working in dusty atmospheres. It
causes hoarseness and chronic cough.
Carcinoma of the larynx may also present with hoarseness so it
is important to perform a laryngoscopy plus biopsy in
suspected cases.
(3) ACUTE TRACHEITIS AND BRONCHITIS

Cause
Spread of the infection, usually bacterial from the upper
respiratory tract after a cold or influenza.
The inflammation of the mucous membrane may involve the
smallest bronchi, and spread into the alveoli and surrounding
lung, when the condition becomes a bronchopneumonia.
Symptoms and signs

Fever.
Cough with moderate mucoid or purulent sputum.
Substernal discomfort.
(4) CHRONIC BRONCHITIS AND EMPHYSEMA

(CHRONIC OBSTRUCTIVE AIRWAYS DISEASE)
In northern climates chronic bronchitis is a common and dis-
abling disease; it is an inflammation of the small bronchi and
bronchioles resulting in chronic cough and sputum.
The swelling of the bronchial mucous membrane causes
narrowing and obstruction of the airflow, especially on
expiration.
Emphysema is due to distension and destruction of the lung
alveoli from the air-trapping in chronic bronchitis.
Causes
Cigarette smoking is by far the most important cause.
Atmospheric pollution with smoke and sulphur dioxide,
especially in damp foggy climates, plays a part.
Bronchitis is more common in certain occupations, e.g. coal
mining, from the effects of the inhaled dust.
Hereditary factors contribute, for a family history is common.
Infection causes flare-ups of the condition. While infection
may initially be viral, bacterial infection follows, the
organisms being commonly Haemophilus inJluenzae and the
Pneumococcus (Streptococcus) pneumoniae.
Symptoms and signs

Chronic cough and sputum.
Breathlessness.
The mechanics of breathing are disturbed, the patient lifting
his chest instead of expanding it on inspiration, and a 'barrel-
shaped' chest may occur in emphysema.
Relapses are usually due to superadded infection, with
increased cough, the sputum becoming purulent and increased
in volume, and fever.
Severe relapses are characterized by cough, sputum, dyspnoea
and cyanosis.
(5) BRONCHIECTASIS
Bronchiectasis is a dilatation with some destruction of the
bronchial walls, associated with chronic infection. Localized
dilatations occur which may be filled with pus.
Causes
May follow childhood whooping cough.
Conditions where mucus plugs or an inhaled foreign body
cause bronchial obstruction. (The air is absorbed in the alveoli
beyond the obstruction, causing areas of lung collapse. The
surrounding healthy and elastic lung causes traction on the
affected part, resulting in bronchial dilatation.)
Chronic bronchitis.
Pneumonia.
Symptoms and signs

Cough and the production of large quantities of purulent
sputum.
'Dry' bronchiectasis may present as haemoptysis, sometimes
massive.
Signs include 'moist sounds' heard with the stethoscope over
the affected part of the lung.
Finger clubbing occurs.
(Diagnosis may be confirmed by bronchogram, the radio-
opaque oil outlining the affected bronchi on X-ray.)
(6) PNEUMONIA
Pneumonia is an infection and inflammation of the alveoli of
the lung. The infection is usually bacterial, but virus invasion
of the respiratory tract may be a predisposing factor.
Pneumonia results in impaired oxygenation of the blood
and various degrees of toxaemia.
Legionnaires' disease - a severe pneumonia recently found
to be due to a small bacillus. (The first epidemic was reported
from an American Legion convention in Philadelphia in 1976.)
The disease is spread through the inhalation of water droplets

contaminated with the bacillus (as in showers).
Types
(a) Lobar pneumonia - a whole lobe becomes solid -con-
solidation usually caused by pneumococcus, sometimes
by staphylococcus.
(b) Broncopneumonia - scattered areas of consolidation in
one or both lungs. When there is infection and retained
secretions in the smallest bronchi, the air in the related
alveoli becomes absorbed causing patchy collapse and
infection of the lung substances. Thus broncho-
pneumonia includes:
pneumonia following spread of respiratory tract infec-
tion;
aspiration pneumonia, where it is assumed infected
matter has been inhaled;
hypostatic pneumonia - a complication of bed rest in
elderly patients with cardiac failure or cerebro-
vascular disease, often a terminal event;
postoperative pneumonia - from failure to clear
secretions (but some cases are pulmonary infarction).
(c) Virus pneumonia - pure virus pneumonia without
secondary bacterial infection is rare, but may occur in
influenza.
The organism Mycoplasma pneumoniae, not a true
virus, may cause outbreaks of mild pneumonia in young
adults. Organisms of the group Chlamydia (which have
the characteristics of both viruses and bacteria) cause
psittacosis in birds such as parrots and budgerigars, and
ornithosis in pigeons. Human infection may occur in
those in contact with such birds, causing a type of
pneumonia.
Symptoms and signs

The onset is sudden with shivering and rigor followed by fever.
There is a harsh cough productive of a little 'rusty' sputum,
later purulent.
Breathlessness.
Pleuritic pain.
Cyanosis.
Rapid pulse.
Toxaemia may be severe with delirium, hypotension and
circulatory collapse.
(7) PULMONARY TUBERCULOSIS

Cause
Infection of the lung with Mycobacterium (Bacillus) tubercul-
osis.
Infection is acquired from inhalation of droplets or dust
from the sputum of a person suffering from the disease. The
source in developed communities of infection is usually a
neglected elderly person, or a vagrant or alcoholic, or an
immigrant from an underdeveloped country where tubercul-
osis may be rampant.
Primary infection may cause few symptoms (malaise,
erythema nodosum) or pass unnoticed. Failure to heal may
cause miliary spread. There may be healing with post-primary
reactivation or reinfection involving a small part of the lung,
or spreading to cause tuberculosis pneumonia, or the infection
may become chronic; there is lung destruction with caseation
(formation of cheesy material) and calcification, cavitation
and fibrosis.
Persons with chronic tuberculosis form the important
reservoir of infection and X-ray campaigns are directed
towards detecting them.
(It is a wise precaution to have a chest X-ray of a patient with
chest symptoms and living in poor circumstances, before
admitting him to the general medical ward. A patient with a
history of pulmonary tuberculosis who develops a chest
infection should also be assumed to have a recrudescence of
tuberculous infection until proved otherwise.)
Symptoms and signs
There may be none in the early stages, the diagnosis being
made on chest X-ray.
Cough with sputum which may be mucoid or purulent.

Haemoptysis.
Fever and night sweats.
Weight loss.
(8) ASTHMA
Bronchial asthma is a condition characterized by recurrent
attacks of wheeze and breathlessness. Attacks are due to
airways obstruction from bronchial muscle spasm, and
mucosal swelling and secretions.
Types
Asthma has recently been classified into two clinical groups:
extrinsic asthma and intrinsic asthma.
Extrinsic asthma
Onset is in childhood and there is often a family history of a
predisposition to allergic disorders including asthma, hay
fever, eczema and skin sensitivity. The term extrinsic is used
because an external allergen often precipitates an attack. The
child or adolescent is symptom-free between attacks, which
often become less frequent in adult life.
Precipitating factors include:
(a) Allergy - an allergic reaction to a substance following
inhalation, ingestion or skin contact.
House-dust is a common allergen, probably due to the
presence of a mite which feeds on the scales shed from
human skin, and is found in mattresses and bedding.
Feathers; the hairs from cats, dogs and horses; and
moulds may also provoke asthma attacks.
Pollens are important allergens in the spring and early
summer. Simple contact with plants such as certain prim-
ulas and foods such as shellfish affect some subjects.
(b) Infection - such as a cold or other respiratory infection.
(c) Exposure to cold air.
(d) Psychological factors - emotional upset such as anger, a
broken love affair or domestic crisis (sometimes added to
the above factors) precipitates many an attack of asthma.
Intrinsic asthma
This affects those over 40, wheeze persisting after a chest
infection, and allergic factors may be less obvious. The patient
may never be free of wheeze, and attacks tend to become more
frequent and severe.
Symptoms and signs

Acute wheeze.
Distress with dyspnoea.
'Tightness' of the chest. (The chest tends to become fixed in
inspiration, for the obstruction mainly affects expiration. The
patient feels he cannot get his breath out, and he may be
anxious with a fear of death.)
Cough, with the difficult expectoration of viscid sputum, but
the sputum may be purulent if there is an infective basis for the
attack.
Status asthmaticus with extreme dyspnoea, cyanosis,
confusion and exhaustion - the picture of respiratory failure;
in such cases the bronchioles may be plugged with viscid,
rubbery secretions, and there is danger of death.
(9) CANCER OF THE LUNG (BRONCHOGENIC

CARCINOMA)
Over two-thirds of patients die within a year of the diagnosis
being made, and the overall 5-year survival rate is only 5070.
Causes
The malignant growth arises in a bronchus, and spreads to
involve the lung lymph glands and distant organs, by metastatic
spread by lymphatics or bloodstream.
Most cases are caused by heavy cigarette-smoking (25 or more
a day).
Irritant and 'carcinogenic' substances in tobacco smoke may
act by promoting malignant change in predisposed
individuals. The incidence of lung cancer declines in those who

stop smoking.
Atmospheric pollution plays a minor part.
Symptoms and signs

There are none in the early stages, the diagnosis being made on
chest X-ray.
Middle-aged men are chiefly affected; there is dry cough and
sometimes haemoptysis.
Sputum may become purulent from infection; bronchial
obstruction causes breathlessness and partial collapse of the
lung, pneumonia or lung abscess.
There may be finger clubbing.
Weakness and weight loss are late signs.
Complications
Pneumonia, lung abscess, pleural effusion.
Obstruction of the superior vena cava from spread to the
mediastinum, causing pain, plethora and swelling of the face
and neck.
The recurrent laryngeal nerve may be involved, causing
hoarseness. Metastases in liver with jaundice, or in the brain
with neurological or behavioural signs.
Metabolic effects, including neuropathy with sensory loss and
weakness in the limbs, and ataxia (balance disturbance).
Endocrine effects include a low salt state and hypotension, and
the opposite state from salt-retention, with Cushingoid
features, the tumour producing an ACTH-like hormone.
(10) COLLAPSE OF THE LUNG (ATELECTASIS)
The term atelectasis is used to describe lung collapse following

blockage of a bronchus. Lung collapse also occurs when air
enters the pleural cavity (pneumothorax) and may rarely be
caused by a massive pleural effusion.
Causes
A large bronchus may be blocked by an inhaled foreign body
or retained secretion postoperatively. The air distal to the
obstruction is absorbed, and the affected lobe or lung
collapses.
The same process may occur less acutely when carcinoma
obstructs a bronchus.
Patchy collapse affecting smaller segments of lung again
occurs postoperatively, or in states of coma from retained
mucus due to inadequate depth of respiration, and failure to
cough effectively.
Symptoms and signs

If a lobe, or a whole lung is involved, there is sudden dyspnoea
and cyanosis.
In small areas of collapse there may be only slight breathless-
ness and the symptoms and signs are those of pneumonia.
There is dullness to percussion and diminished breath sounds
over the affected part.
X-ray changes including raising of the diaphragm from
shrinkage of the lung. (Pulmonary embolism and infarction
may cause a similar picture, sometimes with pleural pain and
haemoptysis.)
(11) SPONTANEOUS PNEUMOTHORAX

Pneumothorax is the presence of air in the pleural cavity,
causing partial or complete collapse of the underlying lung.
Causes
Rupture of a lung alveolus. While a distended area of lung in
emphysema, an emphysematous 'bulla', may be responsible,
in most cases the underlying lung is normal and the reason for
the occurrence of pneumothorax obscure.
Symptoms and signs

The condition is commonest in young men, and may occur
when quietly at rest or on respiratory effort in running or
blowing a wind instrument.
DIFFERENTIAL DIAGNOSIS OF COUGH

Severity Character Productivity
Chronic variable - mild paroxysmal at tenacious mucoid

bronchitis in summer, severe times; more or mucopurulent
in winter marked during sputum
night or on rising
Bronchogenic mild at first, may frequent but mucoid or

carcinoma become severe usually not mucopurulent
paroxysmal sputum; non-
productive at times
Pulmonary becomes severe initially dry and mucopurulent

tuberculosis hacking; frequent sputum (often
but usually not green)
paroxysmal
Bronchiectasis Variable - mild, prolonged copious purulent

moderate or paroxysms; more sputum
severe marked on rising,
lying or bending
Pneumococcal mild at. first; paroxysmal sputum tenacious,

lobar pneumonia becomes severe at times mucoid and 'rusty';
become loose and
mucopurulent
Acute severe in paroxysmal maybe copious

tracheobronchitis pertussis and at times in mucoid sputum,
influenza influenza productive at times
in influenza
Presence Associated signs and Main investigation

of blood symptoms findings
haemoptysis progressive exertional X-ray normal or reveals

uncommon dyspnoea; roughened breath increased hilar markings;
sounds; transient expiratory emphysematous changes
wheezes; fine moist rales;
paranasal sinusitis and
posterior rhinitis often present
blood-streaked weakness; malaise; chest X-ray - new density or

sputum; frank pain; weight loss; mediastinal widening, without
haemoptysis anaemia; hoarseness; calcification (diagnosed
common localized wheezing by bronchoscopy)
haemoptysis fever; night sweats; tuberculin test positive;

common (massive weakness; weight loss; sputum or gastric culture
haemorrhage fine and medium moist rales, positive; X-ray will show
occasional) mostly over upper lung; patchy infiltrates with
cavernous breath sounds areas of fibrosis or
over cavities cavitation
some haemoptysis fever absent; medium or sputum with pus cells;

common coarse moist rales and dilatations on bronchogram
rhonchi; amphoric breath diagnostic
sounds over dilated
bronchi; clubbing of fingers
may occur; intermittent
pneumonia
'rusty' sputum marked fever and X-ray shows opacity of

(degraded blood); prostration; headache; involved lobe; pneumococci
frank haemoptysis dyspnoea; cyanotic at often cultured from
uncommon times; pleuritic chest pain; sputum and blood
signs of consolidation and
moist rales over involved
lobe; pleural friction rub
haemoptysis fever; generalized aching in very marked leukocytosis

rare influenza; coryza, in pertussis; leukopenia often
rhinorrhoea and conjuncti- in influenza; positive
vitis in influenza and culture in pertussis
measles
DIFFERENTIAL DIAGNOSIS OF DIFFICULTV IN

BREATHING: DYSPNOEA
Dyspnoea Character oj breathing
Laryngitis/ tracheitis persistent; usually only prolonged, noisy inspiration

on inspiration
Emphysema at first exertional; persistent prolonged expiration;

in advanced cases audible wheezing ronchi
Pneumonia persistent rapid and shallow; jerky

expiratory grunting in lobar
form
Bronchial paroxysmal with acute prolonged expiration;

asthma attacks audible wheezing
Pneumothorax persistent rapid; shallow

Associated signs and symptoms X-ray changes
usually barking painful cough; loud X-ray normal

inspiratory stridor; hoarseness
usually non-productive cough, may be X-ray shows hyperlucent lung fields,

productive on awakening; cyanosis may depressed diaphragm
be marked; fixed chest
severe harsh cough, mucopurulent sputum; X-ray shows diffuse bilateral density
cyanosis may be marked; signs of of lung tissue in pneumonias;
consolidation, marked pleuritic pain opacification of consolidated lobe in
and prostration in bacterial lobar bacterial lobar pneumonia
pneumonia
cough - at first non-productive, then sticky X-ray shows normal or hyper-

mucoid sputum; cyanosis may be marked; inflated chest; eosinophils in
prolonged high-pitched expiratory sounds sputum and blood
and wheezes; often sneezing
cyanosis; decreased breath sounds; tracheal X-ray shows 'gas' in peripheral lung
deviation; hyperresonance on affected side area
DIFFERENTIAL DIAGNOSIS OF CHEST PAIN

ON BREATHING
Character Location Duration
Acute pleurisy sharp and jabbing lower lateral chest usually few
only on breathing days
Pneumonia sharp and jabbing over involved several days

only on breathing lobe; usually lower
lateral chest
Lung abscess usually sharp and over abscess several days

jabbing only on
breathing; at times
dull and aching
Pneumothorax sharp and jabbing; lower axilla hours to
may be continuous; or under scapula days
intensified by
breathing
Cancer sharp and jabbing over lesion or few days;

only on breathing; course of involved prolonged with
also dull and segmental nerve tumour mass
aching with
tumour mass
Breathing Cough Associated signs

and symptoms
shallow and rapid non-productive fever; pleural friction rub

(proportional to
pain)
severely severe and fever; pleural friction rub;

dyspnoeic hacking; sputum rales; signs of
blood stained or consolidation; (pain prominent
purulent in bacterial pneumonia; not a
feature of diffuse viral
pneumonia)
shallow copious sputum, fever; pleural friction rub;

(proportional purulent, often rales; dullness to percussion;
to pain) foetid and/or may follow aspiration
bloody
persistently ordinarily diminished breath sounds;
dyspnoeic absent tympanitic or flat to percussion
shallow frequent with pain of rib fracture

(proportional to bronchial reproducible; rales with
pain); dyspnoeic lesion obstructive pneumonia and
with obstructive abscess
pneumonia
Sudden severe pain or discomfort as something is 'felt to give'

and breathlessness. (Breathlessness usually improves in a few
minutes, except on the rare occasions when the opening
between lung and pleural cavity is valvular, allowing air in but
not out, and causing 'tension' pneumothorax.)
Most cases are relatively mild and the patient may delay
seeking medical advice. Examination reveals poor expansion
on the affected side, and hyper-resonance on percussion.
(12) DISORDERS OF THE PLEURA

PLEURISY AND PLEURAL EFFUSION
Pleurisy is inflammation of the pleural membrane and may be
'dry' or accompanied by pleural effusion - fluid in the pleural
cavity.
Causes
Usually there is underlying disease:
Lobar pneumonia.
Pulmonary infarction.
Lung cancer or pleural metastases.
Tuberculosis.
Rarer causes are virus infection of the chest wall and collagen
diseases such as rheumatoid arthritis.
In effusion, the fluid may be an inflammatory exudate, con-
taining cells and protein, or a transudate, a watery fluid
formed as a reaction to the underlying disease.
Pleural effusion may accompany oedematous states such as
heart failure, nephrotic syndrome and cirrhosis of the liver.
Empyema is a collection of pus in the pleural cavity; it may
complicate lobar pneumonia from spread of pneumococcal
infection, but is rare with effective antibacterial therapy.
Symptoms and signs

Pain, worse on deep breathing, occurs in dry pleurisy due to
the rubbing-together of the inflamed surfaces and a 'pleural
rub' may be heard with the stethoscope.
Large effusions cause breathlessness.

Dullness on percussion over the effusion.
In empyema, the patient is usually toxic and ill, with a swinging
fever.
Further investigations
Chest X-ray confirms the presence of fluid.
Diagnostic aspiration of fluid - clear and straw-coloured if
transudate.
May be cloudy if infected, or pus with empyema.
Blood-stained often in carcinoma and sometimes in
pulmonary infarction.
Chapter 5
The Gastrointestinal System
Gastrointestinal diseases are the cause of more than 100,70 of all

hospital admissions and medical consultations. Acute infec-
tions such as gastroenteritis are the commonest cause of
medical consultation; appendicitis the commonest cause of
emergency surgery; and carcinoma of the stomach, large
intestine or rectum the most frequent cause of death from
diseases of this system. In the young gastroenteritis can be
lethal; in the mature patient gastrointestinal disturbance is a
frequent cause of chronic disability, and in the elderly
malignant disease of the system causes 10% of all deaths.

(A) weight and fluid balance, diet and output chart;
(B) X-rays: e.g. using contrast medium (as in barium meal,
swallow and enema);
(C) visualization of specifically affected part: e.g. oeso-
phagoscopy, gastroscopy, sigmoidoscopy, proctoscopy;
(D) biopsy;
59
(E) bacteriology (stool samples, etc.);

(F) blood tests (for electrolyte levels and anaemia, etc.);
(0) examination of the mouth.
Common symptoms of gastrointestinal disease will be:

(1) anorexia,
(2) indigestion,
(3) nausea, vomiting and/or diarrhoea/constipation,
(4) pain,
(5) vomiting or passing of blood,
(6) loss of weight.
(A) WEIGHT
The body weight of the patient at the time of the illness, com-
pared to either previous known weight or standard tables (see
table) indicates the extent and duration, or effect, of the
disease. Weight loss may be crucial in the newborn from the
dehydration of gastroenteritis; in the chronically suffering
patient weight loss may indicate a malignant disease and give
objective assessment for the complaint of anorexia. Fluid
balance, input and output charts are essential for assessing
medication or i. v. needs in the vomiting patient.
(B) X-RAYS
Straight abdominal X-rays reveal gas levels in obstruction;

contrast media X-rays reveal partial obstruction, dilatation,
ulceration or disorders in the normal anatomy of the
oesophageal, gastric, duodenal or intestinal outline.
(C) VISUALIZATION
Due to the benefits of fibre-optics, gastroscopy for example,
along with other similar investigations, are much more easily
and effectively performed than ever previously. They can all
now be performed as outpatient procedures and enable the
physician to undertake a biopsy of the apparently disordered
tissues.
THE GASTROINTESTINAL SYSTEM 61
HEIGHTIWEIGHT TABLES FOR ADULT MEN AND

WOMEN
Height Small frame Medium frame Large frame
(in shoes)
ft ins /bs /bs /bs
ADULT MEN
5 2 112-120 118-129 126-141

5 3 115-123 121-133 129-144
5 4 118-126 124-136 132-148
5 5 121-129 127-139 135-152
5 6 124-133 130-143 138-156
5 7 128-137 134-147 142-161
5 8 132-141 138-152 147-166
5 9 136-145 142-156 151-170
5 10 140-150 146-160 155-174
5 11 144-154 150-165 159-179
6 0 148-158 154-170 164-184
6 1 152-162 158-175 168-189
6 2 156-167 162-180 173-194
6 3 160-171 167-185 178-199
6 4 164-175 172-190 182-204
ADULT WOMEN
410 92- 98 96-107 104-119

4 11 94-101 98-110 106-122
5 0 96-104 101-113 109-125
5 1 99-107 104-116 112-128
5 2 102-110 107-119 115-131
5 3 105-113 110-122 118-134
5 4 108-116 113-126 121-138
5 5 111-119 116-130 125-142
5 6 114-123 120-135 129-146
5 7 118-127 124-139 133-150
5 8 122-131 128-143 137-154
5 9 126-135 132-147 141-158
5 10 130-140 136-151 145-163
5 11 134-144 140-155 149-168
6 0 138-148 144-159 153-173
Weights include indoor clothing
(D) BIOPSY
Microscopic sections of tumour, gastric or intestinal wall,
serve to diagnose the cause of the disorder.
(E) BACTERIOLOGY
Bacteriology of stool samples, as well as testing for the
presence of blood and intestinal parasites, reveals the presence
of infective organisms and indicates the necessary treatment.
(F) BLOOD TESTS

To assess the anaemic or infective status, and the physiological
status (e.g. electrolytes, liver function tests, etc.), blood tests
are an important part of the patient's profile.
(G) EXAMINATION OF THE MOUTH

The inspection of the tongue and the mouth is as important as
the examination of the pulse.
The mouth reveals local pathology and the effects of many
general conditions. Adequate fluids, the flow of saliva and the
mechanical cleansing action of mastication, plus sound teeth
and gums, contribute to a healthy mouth. It is an important
part of the nurse's duty to encourage and maintain proper oral
hygiene. Before the patient opens his mouth, conditions of the
lips such as herpes simplex virus infection and accompanying
febrile conditions may be noted. Cracks at the corners of the
mouth (angular cheilitis) are as likely to be due to ill-fitting
dentures as to poor nutrition or vitamin B deficiency.
The normal tongue is moist with somewhat rough surface
from the papillae on it. A dry tongue implies mouth-breathing
or dehydration. A light coating is normal, fur being normally
removed by food and saliva. A furred tongue may simply
indicate that the tongue is not being used much; marked
furring occurs in heavy smokers, and in uraemia (renal
failure). A smooth tongue (glossitis) is an atrophy of the
papillae. A smooth pale tongue suggests anaemia, and in
pernicious anaemia (vitamin B12 deficiency) the tongue may be
sore. A fiery red or magenta tongue occurs in other B vitamin
deficiencies, sometimes due to intestinal malabsorption. The
tongue may show a tremor in alcoholism or Parkinson's
disease. Carcinoma of the tongue may present as a painful,
non-healing hard ulcer.
Dental decay (caries) is very common. Bacterial action on
sugary foods and sweets produces acids which destroy the
enamel, especially if sweets are eaten between meals and brush-
ing of the teeth is neglected. Fluoride in the water supply is
protective. In adults, periodontal disease with inflammation at
the gum margins (gingivitis) is common, and there may be a
mixed bacterial infection. Severe bleeding after dental extrac-
tion suggests a disorder of blood clotting such as haemophilia.
Bleeding of the gums occurs in scurvy (vitamin C deficiency)
and in purpura and blood disorders such as leukaemia (exces-
sive white cells) and agranulocytosis (lack of white cells),
where there may also be ulceration.
Long-term treatment with phenytoin in epileptic patients
may lead to swollen, hypertrophic gums. In lead poisoning, a
blue line forms on the gums.
Stomatitis is inflammation of the mucous membrane of the
mouth. There are many causes; prolonged fever and general-
ized illnesses with poor nutrition and lack of oral hygiene
contribute to its development.
Thrush is an infection with the fungus Candida (Monilia)
albicans and occurs where immunity is lowered, often in
patients who have had steroids or broad-spectrum antibiotics
such as tetracycline which destroy bacteria but allow monilia
to flourish. There are white patches on a sore inflamed mucous
membrane; removal of these fungal patches leaves a raw
bleeding surface. Thetongue,gumsandthroatmaybeinvolved.
Aphthous ulceration is recurrent crops of shallow ulcers of
uncertain cause, often related to emotional stress.
Mouth ulceration occurs in skin diseases such as lichen
planus and in blood diseases such as leukaemia and angranulo-
cytosis.
Common Disorders of the Gastrointestinal

System
(1) DYSPHAGIA (DIFFICULTV IN SWALLOWING)
The oesophagus (gullet) is a muscular tube about 25 cm (to in)
long connecting the pharynx with the stomach and lying for
much of its course in the mediastinum behind the root of the

lung and the heart. It ends just below the diaphragm at the
'cardia', the name given to the junction of oesophagus and
stomach.
Causes
Painful conditions of the mouth and throat.
Swallowed foreign body.
Carconoma of the oesophagus, or involvement by extrinsic
growths.
Stricture from corrosive fluids or following reflux
oesophagitis and hiatus hernia.
Failure of relaxation of the muscle at the lower end of the
oesophagus from atrophy of nerve endings here.
Neurogenic causes, such as bulbar palsy, or after strokes.
Emotional- the 'lump in the throat' feeling, at times of stress.
Myasthenia gravis, a rare condition with muscle weakness.
Symptoms and signs

In any form of obstruction, the patient can usually point
accurately to its site.
The swallowing of solids becomes progressively more difficult;
ultimately only liquids can be passed.
There is considerable loss of weight and emaciation.
Attempts at swallowing are followed by regurgitation of the
food.
Following a stroke there may be transient dysphagia, but only

after bilateral upper motor neurone involvement is there
persistent disturbance of the swallowing mechanism, with risk
of regurgitation of food into the lungs.
These include barium swallow X-ray, oesophagoscopy and
biopsy.
(2) HIATUS HERNIA AND REFLUX OESOPHAGITIS
A hiatus is an opening, and a hernia is a protrusion of a viscus
known in lay terms as a 'rupture'. In hiatus hernia, part of the
stomach slides up through the diaphragmatic hiatus, or less
commonly rolls up alongside the oesophagus, into the thorax.
If the sphincter between stomach and oesophagus becomes
incompetent, reflux of acid gastric juice has an irritant effect
on the mucous membrane of the lower oesophagus causing
oesophagitis, and stricture in severe cases.
Symptoms and signs

Heartburn and retrosternal pain.
Feeling of fulness and flatulence.
Symptoms are worse on lying down or stooping.
Acid regurgitation, vomiting and dysphagia may occur.
Anaemia may be due to oozing of blood from erosion or
ulceration.
Barium X-ray shows the hernia, or allows demonstration of
reflux.
(3) GASTRITIS
The stomach is a muscular organ which breaks up and mixes
food; the mucous membrane contains cells secreting hydro-
chloric acid and pepsin which contribute to digestion.
Acute gastritis is an inflammation of the mucous membrane
of the stomach.
Causes
Ingestion of irritant substances such as alcohol, aspirin.
Food poisoning. There is discomfort or pain, nausea and
vomiting, usually settling in a day or two if further irritation is
avoided.
(4) PEPTIC ULCER

(A) ULCERATION
A peptic ulcer is a hole in the mucous membrane of a part of
the gastrointestinal tract to which gastric juice, hydrochloric

acid-pepsin, has access.
Types
Gastric ulcer occurs in the stomach usually on the lesser (inner)
curvature.
Duodenal ulcer occurs in the first part of the duodenum, just
beyond the pyloric outlet of the stomach.
Causes
Peptic ulcer tends to run in families, suggesting a genetic
predisposition.
The mucous membrane is normally resistant to the action of
hydrochloric acid and pepsin. Ulceration occurs when the
acid-pepsin versus mucosal resistance balance is disturbed. In
duodenal ulcer there is a high acid-pepsin production from
excess secreting cells in the stomach. In gastric ulcer the acid
secretion may be high or low, and decreased mucosal
resistance may be more important.
Mucosal resistance is lowered by heavy cigarette-smoking,
alcohol, and certain drugs. (Thus aspirin may cause acute
erosions and bleeding; phenylbutazone and indomethacin,
used in the treatment of rheumatoid arthritis, cause gastric
ulceration though persons with chronic diseases such as
rheumatoid arthritis may have lowered mucosal resistance.
Factors such as overwork and mental stress cannot be proved

to be causative, but they may exacerbate ulcer symptoms.
Symptoms and signs

The chief symptom is pain, felt in the epigastrium, and the
patient may be able to point with one finger at its site, where
there may be tenderness and resistance to palpation, with
muscle 'guarding'.
It occurs between meals, is relieved by food and alkalis and
often occurs in the middle of the night, around 2 a.m., waking
the patient from sleep.
It has a characteristic periodicity, occurring over a few days or
a week; then the patient may remain symptom-free for weeks
or months.
Vomiting.
Haemorrhage and perforation.
Melaena.
Barium meal X-ray and screening shows an ulcer crater or
duodenum deformity.
Gastroscopy (and duodenoscopy) using the flexible fibre-
optic instrument permits a direct view with little discomfort to
the patient, allows biopsy of gastric ulcer if malignancy is
suspected and is indicated in all cases of X-ray negative
dyspepsia.
(8) COMPLICATIONS
A haematemesis is a vomiting of blood which may be fresh and
red or dark brown and 'coffee-ground' in appearance if altered
by stomach acid.
A melaena is a loose, black, tarry, glistening stool from
blood altered by passage through the alimentary tract, but if
the haemorrhage is severe the stool may contain dark red
blood.
Haematemesis and melaena
Causes
Gastric or duodenal ulcer eroding a blood vessel, and rarely
gastric carcinoma.
Aspirin ingestion, often with another irritant such as alcohol.
(Aspirin provokes bleeding from an existing peptic ulcer and in
addition causes acute erosions, often multiple with oozing of
blood.)
Cirrhosis of the liver with bleeding from oesophageal veins.
Bleeding states, caused by anticoagulants, or in purpura and
leukaemia.
Haematemesis should be differentiated from haemoptysis

(where the blood may be brighter and frothy), from a vomit of
swallowed blood from a nose bleed, and from the vomiting of
gastric contents in pyloric stenosis. If there is doubt, specimens
must be preserved; their volume gives some indication of the
severity of the haemorrhage.
Symptoms and signs

Bleeding may present as haematemesis, melaena or both, or
may be 'silent' into the alimentary tract. The signs are those of
blood loss:
Pallor.
Cold and clammy skin.
Apprehension and restlessness.
Rapid pulse and low blood pressure.
Fainting or collapse.
Dehydration from fluid loss.
Usually there is no pain, but there may have been an exacerb-
ation of ulcer symptoms a few days previously.
Perforation
Cause
The ulcer erodes through the wall of stomach or duodenum
with escape of gastric contents into the peritoneal cavity,
causing severe irritation and peritonitis.
Symptoms and signs

Sudden severe upper abdominal pain.
Tenderness and board-like rigidity of the abdomen.
Rapidly rising pulse.
X-ray shows gas below the diaphragm.
Pyloric spasm and stenosis

Acute exacerbation of the ulcer may be associated with muscle
spasm, so that the stomach does not empty properly and
distends. In chronic ulceration there may be fibrous
contraction at the duodenum beyond the pyloric outlet of the
stomach, pyloric stenosis, with gross hold-up and distension.
Symptoms and signs

The ulcer pain changes its characteristics, now occurring after
meals or in the evening when the stomach is distended.
Increasing weight loss, dehydration, salt and acid loss, and
alkalosis on blood testing.
Gastric aspiration shows residual volumes of Vi-I litre;
barium meal confirms gastric distension.
(5) CARCINOMA OF THE STOMACH

This occurs in the middle-aged and elderly. It should be
suspected in non-healing gastric ulcers.
Symptoms and signs

Upper abdominal pain or discomfort not clearly related to
meals.
Loss of appetite.
Weight loss.
Nausea and vomiting.
Mass may become palpable in the epigastrium.
Anaemia from blood loss.
The first signs may be of metastatic growths in the liver causing
enlargement and jaundice, or in the peritoneal cavity causing
ascites (fluid distension).
Early diagnosis is essential and is aided by:
Barium meal.
Gastric biopsy and gastroscopy.
Stool tests for occult blood, which may be positive.
Small intestine
The small intestine consists of the duodenum, and the jejunum
and ileum lying in coils attached to the posterior abdominal
wall by the mesentery (a fold of peritoneum in which blood
vessels and lymphatics run). The ileum ends in the caecum; the
start of the large intestine (colon) at the right iliac fossa.
The small intestine is concerned with digestion and absorp-
tion of foods, minerals and vitamins, the mucosa being in folds
or villi which greatly increase the absorptive area. Enzymes
secreted by the mucosa split food protein into amino acids;
carbohydrates and sugars into glucose; these are absorbed into
the blood vessels which join to form the portal vein to reach the
liver. Fats are digested by the action of bile salts and pancreatic
lipase, absorbed into lacteals in the villi to reach the
lymphatics, and are carried via the thoracic duct to join the
general circulation in the great veins near the heart.
The terminal part of the ileum contains patches of lymphoid
tissue, Peyer's patches, which become involved in typhoid
infection. The lymphoid tissue may be concerned in the body's
immunity mechanism and the production of antibodies, and
viruses may colonize here before spreading to other tissues,
e.g. poliomyelitis.
(6) GASTROENTERITIS
This is caused by bacterial toxins, Clostridia, Salmonella

and other infections. They include typhoid and paratyphoid
(enteric fever), food poisoning, dysentery and cholera.
TYPHOID AND PARA TYPHOID

Cause
Bacillus typhoid, and B. paratyphoid A, B and C (milder
infection). These organisms belong to the Salmonella group.
Mode of infection
Faecal contamination frQm a patient or carrier, who may be
symptomless. Water and foods such as meat products and milk
transmit the infection where hygiene is poor.
Symptoms and signs
Typhoid is initially a bloodstream infection and during the
first week the symptoms are not gastrointestinal, but systemic
ones:
Fever.
Pulse slow in relation to the temperature.
Headache.
Weakness.
Fatigue.
Rose-spot rash of the abdomen.
There is constipation rather than diarrhoea at this stage and
diagnosis may be difficult unless the condition is borne in
mind.
Blood culture is positive during the first 10 days, and white cell
count shows decreased polymorphs, instead of the increase in
most infections.
If the condition is allowed to proceed, the patient becomes
extremely ill with diarrhoea, pea-soup stools, abdominal
distension and risk of bowel haemorrhage and perforation.
Stool culture is then positive.
Diagnosis may be confirmed by the Widal agglutination test,
which demonstrates the presence of the antibodies that
develop after 2-3 weeks.
FOOD POISONING
Causes
Salmonella organisms:
Campylobaeter organisms (from poultry and cattle) have
recently been implicated in human enteritis.
Bacillus (Clostridium) welehii.
Staphylococcal - from preformed toxin.
Botulism.
The food poisoning Salmonella are pathogens of men and

animals, and poultry, so that infection is acquired from human
and animal cases, and meat and poultry products such as
improperly cooked broiler chickens.
Symptoms and signs

These organisms are not invasive like the typhoid ones and
cases present with gastric or intestinal symptoms rather than
generalized disease, about 24 hours after infection:
Abdominal pain.
Vomiting and diarrhoea.
Fever and malaise.
Clostridium welchii grows in improperly cooked or reheated
meat and symptoms start usually with diarrhoea 8-24 hours
after ingestion.
The staphylococcal toxin is formed when the organisms
multiply in food contaminated with pus from a food handler
with a boil or abscess, or staphylococcal nasal discharge, and
vomiting occurs 2-5 hours after the infected meal.
(7) DYSENTERY
BACILLARY DYSENTERY
Cause
Bacilli of the Shigella group, of which Sh. sonnei is much the
commonest, though other organisms cause more severe
dysentery, especially in the tropics. They are purely human
pathogens, causing inflammation of the large bowel (colon).
Mode of infection
From the faeces of cases, and carriers, usually by the hands,
from objects such as lavatory seats. This is how Sonnei dysen-
tery spreads in nursery schools, where infection is common,
and in hospital wards. Contamination of food and water may
cause epidemics.
Symptoms and signs
Lower abdominal discomfort.
Fever and diarrhoea often with blood mucus in the stools.
Malaise from toxaemia in severe cases.
AMOEBIC DYSENTERY
This is due to bowel infection with the small parasite
Entamoeba histolytica, which occurs in the tropics and spreads
in cystic form from the stools. There is diarrhoea with bleeding
and bowel ulceration, but the symptoms may be mild. There
may be spread to the liver, causing amoebic abscess, which
may discharge through the diaphragm and be coughed up as
pus. A fluorescent antibody test in the blood may be helpful.
CHOLERA
This disease is caused by a bacillus (Vibrio) spreading by
contamination of water supplies. It is a fulminating bowel
infection, with copious fluid 'rice-eater' stools.
CROHN'S DISEASE (REGIONAL ILEITIS)

This is a relapsing inflammatory disorder of areas of the small
intestine, usually the terminal ileum; the colon and anus may
also be involved. The cause is unknown but there is a familial
incidence, the disease affecting mainly young adults.
Symptoms and signs

Abdominal pain.
Diarrhoea.
Lack of appetite.
Weight loss and fever.
Acute episodes may simulate acute appendicitis with pain and
tenderness at the right iliac fossa.
May be intestinal obstruction with vomiting and a palpable
mass or peritonitis.
The stools may contain blood or be fatty (steatorrhoea) with

malabsorption from the lower ileum.
Anaemia.
Diagnosis may be confirmed by narrowing of terminal ileum
on barium 'follow-through'.
(8) MALABSORPTION SYNDROME

This is a group of conditions in which absorption of foods
through the small intestine is impaired. Fat absorption is
especially impaired, but carbohydrates, proteins, minerals and
vitamins are also poorly absorbed, in varying degree.
Steatorrhoea means frequent, pale, greasy, bulky and
offensive stools which float in the toilet and are difficult to
flush away.
Causes
Lesions of the small intestine
Coeliac disease occurs in children (failure to thrive, 'pot-belly'
and rickets).
Coeliac syndrome or idiopathic steatorrhoea is the adult
equivalent. These conditions are due to an intolerance to the
protein fraction called gluten in wheat and rye flour.
Tropical sprue occurs in certain zones especially in the Far
East, but may persist on return to temperate climate.
Crohn's disease and infiltrations of the intestine in conditions
such as Hodgkin's disease and blood disorders, tuberculosis,
and amyloidosis also cause malabsorption.
Lack of digestive enzymes or bile salts

E.g. chronic pancreatitis and obstructive jaundice. Intestinal
lactase deficiency is of importance in causing failure of
digestion of lactose (milk-sugar) with resultant intolerance to
milk.
After surgical operations

E.g. gastrectomy, massive resections of intestine, and with
'blind-loops' which often harbour bacteria which utilize
nutrients and impair digestive action.
The parasite Giardia lamblia may cause malabsorption in
children.
Symptoms and signs

Steatorrhoea.
Weight loss.
Anorexia and distended abdomen.
Anaemia is a common presentation from deficiency of iron,
folic acid and vitamin B.
Other vitamin B deficiencies cause sore red tongue and
peripheral neuritis.
Osteomalacia (the adult equivalent of rickets) due to lack of
vitamin D and calcium, causes bone thinning and fractures.
Bleeding tendency due to lack of vitamin K.
Oedema and ascites due to hypoproteinaemia.
Low blood potassium causes further general weakness.
Faecal fat estimation - stools are collected for 3-5 days on a
normal ward diet; with steatorrhoea, faecal fat output exceeds
6g per 24h.
Glucose tolerance test - in malabsorption the blood sugar
curve is 'flat' after 75 g oral glucose, but the test is not reliable
in chronic pancreatitis where there may be associated diabetes.
Xylose absorption test - xylose is a sugar which in normal
people is absorbed but not metabolized so it is excreted
unchanged in the urine. In malabsorption, 25 g is given by
mouth and less than 20070 appears in the urine in 5 h.
Barium meal and follow-through shows a 'clumping' pattern.
Intestinal biopsy - a small metal capsule attached to a thin
plastic tube, is swallowed, preferably in the evening so as to
pass into the small intestine by the next morning, its position
being verified on X-ray. A syringe is attached to the tubing
(which has been fixed at the mouth) and suction triggers off a
tiny cutting edge in the capsule, into which a minute piece of
intestinal mucosa is drawn. The device is then slowly with-
drawn through the mouth, and the biopsy specimen examined.
In coeliac disease and some of the other conditions, the villi are
deformed and flattened.
Other investigations are directed towards the anaemia and
include serum levels of iron, folic acid and B12.
Mineral lack may be detected by serum calcium, phosphorus
and alkaline phosphatase tests, and by X-rays of bones. The
serum potassium may be low. Protein deficiency results in a
low serum albumin.
The large intestine (caecum, colon and rectum)

The large intestine starts at the caecum (from which protrudes
the appendix) in the right iliac fossa, then becomes the
ascending, transverse and descending colon, and pelvic or
sigmoid colon, rectum and anal sphincter. The external
muscular layer is collected into three longitudinal bands which
are shorter than the rest of the colon, causing puckering or
'haustration'. The function of the colon is the absorption of
water and minerals, converting the intestinal contents to semi-
solid faeces (about 150 g daily). The rectum is normally empty,
faeces entering causing stimulation and defaecation of the
pelvic and descending colon contents. The colon normally
contains Escherichia coli and large numbers of other bacteria
which may cause serious disease in tissues outside the colon.
(9) CONSTIPATION
Constipation is the infrequent and difficult passage of hard
faeces. Most people have a bowel action daily, normal 'habit-
time' being after breakfast as the result of the gastrocolic reflex
stimulus. There is, however, considerable variation, some
people normally having a motion only three or four times per
week.
Causes
Failure to answer the call to stool - this may be due to
inadequate time at breakfast, lack of toilet facilities, forced
use of the unpleasant bedpan, or physical weakness in the
elderly. Fluid becomes absorbed from the stools in the rectum,
resulting in hard motions or faecal impaction.
Abuse of purgatives - after powerful purgation, the whole
colon may empty, take a day or two to refill so that further
purgation is taken to attempt to produce a motion. The bowel
may become dependent on such stimulation, and true constip-
ation follow its withdrawal.
Dietary - a large part of the faeces is in fact of non-dietary
origin; however, inadequate bulk in the diet and lack of fluids
may cause constipation.
General illness, especially febrile illness, and bed rest with lack
of exercise is a possible factor. Depressive states and
myxoedema (hypothyroidism) are also causes.
Disorders of the colon
Carcinoma: change in bowel habit, i.e. constipation in

someone previously regular, should raise suspicions.
Adhesions after operation.
Anal fissure making defaecation painful.
Symptoms and effects

The only symptoms of constipation are vague loss of appetite
and abdominal discomfort, due to distension.
Constipation is, however, important in the elderly for it may
result in faecal impaction in the rectum and spurious
diarrhoea, a little watery faeces being squeezed past the
obstruction; impaction may also cause both faecal and urinary
incontinence.
A heavy loaded colon may press on pelvic veins, worsening
varicose veins in the leg, and possibly contributing to venous
thrombosis. Urinary tract infections may be commoner if
there is constipation, the mode of infection being uncertain.
Straining at stool worsens haemorrhoids and is undesirable in

those with cardiac and respiratory disease.
(10) DIARRHOEA
Diarrhoea means the passage of frequent or loose stools. After
defaecation in some cases there may be a residual feeling of
unsatisfactory evacuation or 'tenesmus'.
Causes
(A) Acute
(1) Gastrointestinal infections
(a) food poisoning, as part of gastroenteritis;
(b) typhoid and paratyphoid;
(c) dysentery - stools contain blood and mucus, and are
often watery;
(d) cholera - profuse 'rice-water' stools with little faecal
matter.
(2) Melaena from bleeding peptic ulcer, aspirin ingestion, or
oesophageal varices - stools loose, black and tarry.
(3) Excessive use of broad-spectrum antibiotics such as tetra-
cycline, which cause upset in the normal bowel bacterial
flora.
(B) Recurrent or chronic

(1) Small intestine
(a) malabsorption syndrome - steatorrhoea (fatty stools);
(b) Crohn's disease - stools loose and may contain blood,
or steatorrhoea.
(2) Large intestine
(a) irritable colon syndrome;
(b) diverticular disease;
(c) ulcerative colitis;
(d) carcinoma.
(3) General causes
anxiety and 'nerves';
thyrotoxicosis (hyperthyroidism);
diabetes - nocturnal diarrhoea;
pellagra (a vitamin B factor, nicotinamide, deficiency).
The stool must always be inspected, and sent for bacterio-
logical investigation if there is any suspicion of an infective
cause. Occult blood tests and faecal fat estimation may also be
required; sigmoidoscopy, barium enema or barium meal and
follow-through.
Effects of diarrhoea
Severe diarrhoea is debilitating (and may be fatal in infants).
Large amounts of fluid, sodium and potassium may be lost
leading to hypovolaemia, hypokalaemia, and collapse.
Nutrients are lost in the steatorrhoea of malabsorption, and
blood in melaena.
(11) IRRITABLE COLON SYNDROME (SPASTIC COLON)

This is an ill-defined disorder presenting as frequency of bowel
movement, or urgency after meals - suggested causes include
over-active gastrocolic reflex, intestinal hurry from lactase
deficiency (when removing milk from the diet may help) and
disturbance of motility of the large bowel, and anxiety.
(12) DIVERTICULAR DISEASE OF THE COLON
Diverticulosis is the presence of little 'pouchings' of mucous

membrane through the muscular wall, where blood vessels
enter, of the pelvic and descending colon.
Causes
A disturbance of motility, often with muscle thickening.
Chronic low-grade infection, related possibly to chronic
anxiety and tension.
Related to lack of bulk (fibre) in the diet, for the disorder is
rare in underdeveloped countries.
Symptoms and signs

Abdominal discomfort.
Colicky pain at the left lower abdomen.
Altered bowel habit.

Episodes of constipation or large bowel obstruction.
Distension and later vomiting.
Tenderness, fever and malaise.
A mass may become palpable from peri-diverticular abscess,
and there may be perforation with peritonitis, or fistula
formation.
These may include barium enema; sigmoidoscopy.
(13) ULCERATIVE COLITIS

This is an inflammatory disease of the large intestine. It may be
confined to the rectum and pelvic colon, or the whole colon
may be involved. There is patchy ulceration and bleeding of
the mucous membrane, and in late stages fibrosis and
shortening of the bowel. Ulcerative colitis occurs in young and
middle-aged adults and is slightly commoner in women.
Cause
The cause is unknown.
'Autoimmunity' has been suggested; the body destroying its
own tissues. Some patients have been found to have antibodies
to cows' milk in their blood and a few patients have lactase
deficiency in the small intestine, but in most cases milk sensi-
tivity seems to have little bearing on the condition.
Psychosomatic factors have been involved - these include
tense personality, insistence on precision and tidiness, and
.repression of emotional feelings, the bowel 'losing its temper'
instead.
Symptoms and signs

Episodes of diarrhoea, often with blood and mucus in the
stools, which may amount to about a dozen loose motions
daily.
Tenesmus (persistent desire to defaecate) and the patient is
afraid to go far from a toilet.
(There are remissions in which bowel movement may return
towards normal but relapses tend to occur over months or
years.)
Fulminating attacks of bloody diarrhoea are associated with
fever, emaciation and anaemia.
Complications
Complications include bowel abscess, stricture and perfor-
ation. Where the whole colon is involved, toxic dilatation and
rupture may occur, and in long-standing cases there is an
increased risk of carcinoma. Ulcerative colitis may also have
systemic complications including skin sepsis and abscesses,
erythema nodosum, arthritis (which may involve spinal joints),
spondylitis, iritis, liver inflammation and cirrhosis, and a
tendency to venous thrombosis.
Stool bacteriology - to exclude infections.
Sigmoidoscopy - this is an examination through the rectum.
The mucosa is red, granular and bleeds easily and there may be
mucus or a mucopurulent exudate.
Barium enema shows an irregular or ulcerated mucosal
pattern, loss of haustrations, and in late stages a tube-like
colon. Straight X-ray may show toxic dilatation in acute cases.
Blood examination may show anaemia, raised white cell count
and ESR, and fluid and electrolyte depletion, especially a low
potassium, from prolonged diarrhoea.
114) CARCINOMA OF THE RECTUM AND COLON

Carcinoma of the large bowel is common (causing some 15 000
deaths annually in Britain) and therefore being second only to
carcinoma of the bronchus in terms of mortality from cancer.
The disease is most frequent in the middle-aged and elderly,
but can occur in young people.
Symptoms and signs

Cancer of the rectum is commonest, symptoms include:
Bleeding (often mistakenly ascribed to piles);
Change of bowel habit, often with diarrhoea and passage of
slime;
The cancer may be palpable with the finger on rectal examina-
tion (cancer of the pelvic colon presents similarly);
In the descending and transverse colon, the change of bowel
habit is likely to present as constipation rather than diarrhoea,
and there may be stricture and obstruction with abdominal
distension and later vomiting;
Growths in the caecum and ascending colon may be silent, the
complaint being of vague deterioration in health, weight loss,
and weakness from anaemia due to occult bleeding;
A mass may become palpable in colonic cancer in later stages;
Sometimes the growth presents as metastases in the liver with
jaundice, or as ascites.
Further investigations include stool tests for occult blood,
sigmoidoscopy and barium enema. Blood examination may
show anaemia and raised ESR. Laparotomy (surgical explor-
ation of the abdomen) may be indicated in suspicious cases
even when barium enema is negative.
(15) THE ACUTE ABDOMEN

When confronted with a patient with abdominal pain and
vomiting, the decision as to whether the condition is a
'surgical' one requiring operation may not be possible without
careful observation and charting of pulse and temperature.
Diabetic ketosis may present with abdominal pain and
vomiting, operation is lethal in this situation, and the urine
must be routinely tested for sugar and ketones to exclude it.
Analgesics to relieve pain may obscure diagnosis of the acute
abdomen, and should only be given when the course of
management has been decided. In doubtful cases, it may be
necessary to proceed to laparotomy.
(a) Acute appendicitis is commonest in children and young
adults, but may occur in the elderly.
Symptoms:
central abdominal discomfort;
followed by pain, tenderness and muscle guarding at the
right iliac fossa, slight vomiting;
raised pulse and temperature, but pyrexia may not be
marked. (Mensenteric adenitis is an inflammation of
abdominal lymph glands in children and may have
similar symptoms.)
(b) Perforated peptic ulcer causes severe upper abdominal
pain, tenderness and rigidity.
(c) Acute cholecystitis, biliary colic and acute pancreatitis
cause abdominal pain.
(d) Renal colic causes pain in the loin or iliac fossa - these
conditions are described in later chapters.
(e) Ruptured ectopic pregnancy is a 'gynaecological'
emergency; pregnancy has occurred in the ovarian tube
instead of the uterus, the tube ruptures in the early weeks
causing severe lower abdominal pain and usually vaginal
bleeding. There is a history of a missed period.
(f) Salpingitis, inflammation of the ovarian tubes, is another
cause of lower abdominal pain.
(g) Intussusception is an invagination of one length of
intestine into another; it occurs in infants, and in adults in
association with a lesion such as a polyp or carcinoma.
Symptoms:
pain;
vomiting;
bloody diarrhoea;
palpable mass;
(h) Intestinal obstruction has many possible causes:
herniae caught at the inguinal and femoral canals;
adhesions from previous operations;
carcinoma;
mesenteric arterial thrombosis causing ischaemia and
stasis;
volvulus (sudden twisting) of the bowel in the elderly.
Symptoms include pain and vomiting, but if the large
DIFFERENTIAL DIAGNOSIS OF VOMITING-

Onset and duration Severity and
frequency
Obstructed long after meals, often initially frequent, not
ulcer during night copious
Carcinoma of gradual in onset; may become intractable

the stomach initially only after a and severe
heavy meal; often repeated
bouts with free periods
Alcoholic begins during alcoholic may be persistent and
gastritis excess of next morning; severe
may last several days or
only few hours
Intestinal sudden in onset; severe and frequent,
obstruction persistent until obstruction especially with high
relieved obstruction
Biliary colic sudden in onset often recurrent and severe
Pancreatitis sudden in onset, usually usually not severe or

only an early symptom persistent, but may
persist if ileus develops
Appendicitis an early symptom usually not severe or

persistent
Peritonitis occurs early, and then initially forceful and

recurs when ileus develops severe; later meagre and
frequent
Staphylococcal sudden, 5-6 h after food; severe and frequent;

food poisoning lasts 4-6 h retching and salivation
present
Due to Gastrointestinal Disorders
Associated findings Key laboratory findings
reduction in typical ulcer pain; feeling gastric aspirate - large volume and
of fullness, relieved by vomiting; thirst, retained food particles; obstruction seen
oliguria, succussion splash of stomach on barium studies of stomach;
hypokalaemic alkalosis
epigastric pain; belching; feeling of may be visualized by X-rays and/or

fullness, weight loss, pallor, melaena gastroscopy; cytological study of
often; palpable epigastric mass in some; gastric washings may show tumour
metastatic nodes cells
headache, tremor, epigastric tender- typical lesions seen on gastroscopy and
ness, haematemesis and melaena gastroscopic biopsy
may occur
colicky epigastric or periumbilical pain, X-ray shows fluid level in 3-4 h

constipation, no flatus; may be weak
and shock-like; abdomen soft until
distended then diffusely tender; loud
bowel sounds, visible peristalsis in some
pain in right upper quadrant and radio-opaque stones on flat film in some;
epigastrium, may radiate to right diagnosis often confirmed by
shoulder, causes patient to flex trunk; cholangiogram
belching, cold sweats; fever and chills
if cholangitis; jaundice at times;
abdomen soft
history of alcoholic excess, biliary leukocytosis, elevated serum amylase,
disease or recent surgery; severe often low serum calcium; X-ray may
epigastric pain; wide-ranging tempera- show calcified pancreas or distortion of
ture; tender epigastrium, slightly rigid duodenum
or soft; shock in severe cases
preceded by indigestion or flatulence; leukocytosis; X-ray may show local

periumbilical colic at first in many; distension
then continuous pain and tenderness in
right lower quadrant; rebound tender-
ness and local rigidity in same area;
sometimes local distension; rectal
tenderness in many
finding of precipitating illness; high leukocytosis; X-ray shows ileus and

fever usual; severe pain initially intraperitoneal fluid
diffuse, then often more localized;
intense and rebound tenderness,
diminished or absent bowel sounds;
distension may develop
colicky periumbilical or hypogastric temperature normal, no leukocytosis;

pain; diarrhoea, at times bloody; diagnosis by smear or culture
sweating, prostration, rarely shock; little
or no abdominal distension or
tenderness
DIFFERENTIAL DIAGNOSIS OF DIARRHOEA - 1

Onset and Severity Character Nature of
duration stool
Salmonellosis sudden; mild or straining stools watery with

usually 2-5 severe and tenesmus increased mucus;
days; may be
occasionally present
up to 4 days
Shigellosis sudden; may severe - straining watery, greenish,

last 2-10 20 or more and with increased
days movements tenesmus mucus; blood
a day and pus in
severe cases
Amoebiasis usually mild or tenesmus small, liquid or

gradual; severe; in many semiliquid, with
sudden at frequent, bloody mucus
times; small bowel
chronic or movements
recurrent
Cholera abrupt usually no tenesmus stools watery,

severe or abdominal profuse, flecks
cramping of mucus - no
blood or pus -
'rice water'
Staphylococcal sudden; often mild, or often may be soft

enterocolitis persists severe and 'explosive' with faecal
unless continuous material, or
treated; watery green
death may with blood
occur in
24-48 h
Viral sudden or mild or tenesmus watery

enteritis gradual - severe uncommon diarrhoea; no
lasts from blood, mucus
I day to a or pus
week
Ulcerative usually from 2-3 often soft and

colitis gradual; can to 15-20 nocturnal; mushy or loose,
be abrupt in movements often bloody, mucoid-
fulminating a day tenesmus, pus in most
form; few urgency, severe
weeks to rectal incon-
chronic tinence
Regional gradual, from nocturnal stools soft, semiliquid;

enteritis continuous 2 to 10 at times; watery in very severe;
or recurrent stools a tenesmus bloody pus with colonic
day uncommon disease; bulky foul stools
with small bowel disease
Abdominal Associated signs Key laboratory

findings and symptoms findings
increased abdominal cramping, diagnosis by culture

peristalsis; nausea and vomiting of stool; leukopenia
tenderness present; fever; chills; in some
toxic
increased cramping may be first sigmoidoscopy - red,

peristalsis; symptom; nausea, oedematous mucosa
abdominal vomiting, fever - variable with pinpoint and
tenderness, larger ulcerations;
especially over diagnosis by culture
colon of stool
may simulate may be very toxic leukocytosis marked in

acute appen- with fever and chills; acute; no eosinophilia;
dicitis anaemia, malnutrition, sigmoidoscopy - small,
lethargy punched-out ulcers; exudate
may show parasites or
cysts
abdomen often vomiting late, marked haemoconcentration,

soft; no without nausea; often renal shutdown and
tenderness muscular cramping; uraemia; organisms in
thirst, cyanosis, stool identified by
shock; hypotension; agglutination or
poor skin turgor culture
distended, often begins after haemoconcentration,

with dimini- antibiotics; high fever in hypokalaemia, hypona-
shed bowel some; toxic, drowsy, traemia, hypochloraemia,
sounds in confused; nausea, acidosis; stool smear
severe cases; vomiting, hiccups; and culture on blood
mild, diffuse abdominal pain mild agar will show staphy-
tenderness or absent; signs of lococci; sigmoidoscopy
shock in some will show sloughing
audible cramping is prominent; bacterial flora of bowel

borborygmi; fatigue and dry mouth at normal on culture;
mild onset; malaise, anorexia, blood count and
abdominal nausea; vomiting usually chemistry usually
tenderness; only at onset; fever in normal
increased some; headache,
peristalsis dizziness; flatus increased;
weakness, dehydration
tenderness cramping abdominal sigmoidoscopy - varying

over left pains - left lower degrees of bleeding
colon; quadrant; backache; erythema, ulceration;
peristalsis rectal bleeding; weakness, findings at barium enema
usually normal; anorexia; nausea; nervous; diagnostic; often hypo-
some distension fever in some; anal albuminaemia and
sphincter spastic, often anaemia - no leukocytosis
haemorrhoids and fissures
tender mass in periumbilical cramps, sigmoidoscopy - ulcerations

right lower quadrant often relieved by defae- in some; barium enema
common; may simulate cation; bloati\lg, flatulence; shows colonic involvement,
appendicitis; signs of back pain; fever at times; often segmental; stricture
bowel obstruction at rectal and anal fistulae; formation at times; anaemia
times melaena uncommon and hypoproteinaemia
DIFFERENTIAL DIAGNOSIS OF DIARRHOEA - 2

Onset and Character of Gastrointestinal
severity diarrhoea and symptoms
stools
Gluten gradual; chronic; less than 10 anorexia;

enteropathy variable in movements a day; distension, cramps,
severity usually bulky, flatulence
frothy, steator-
rhoea, but may be
watery
Sprue gradual or acute; often 'explosive', anorexia; nausea

chronic or may awaken and vomiting at
recurrent patient; stool soft, times; flatulence,
bulky, pale- borborygmi
steatorrhoea
Chronic gradual chionic; usually steator- previous episodes

pancreatitis moderate in rhoea; may be of acute abdominal
severity watery pain, often of biliary
disease
Cystic gradual; chronic; 3-6 movements appetite increased,

fibrosis moderate per day; steator- except during
rhoea, almost infections; variable
never watery abdominal pain
Carcinoma gradual; chronic stool often small pain during or after

of rectum or recurrent; and deformed with defaecation;
usually not severe mucorrhoea, constipation at
mixed with blood; times; rectal
often urgency bleeding at times,
and sense of independent of
incomplete defaecation
evacuation
Abdominal signs Associated findings Key laboratory data
some abdominal weakness, weight loss, glos- serum proteins low; anaemia;
distension at sitis, skin and mucosal hypocalcaemia; cholesterol
times bleeding; dependent oedema low; faecal fat increased;
in some; urine volume X-ray - dilated small bowel;
greater at night; tetany segmentation and fragment-
and paraesthesias at times ation of barium, thickening
of folds; jejunal biopsy-
shortening and thickening of
villi
abdomen, often weakness, weight loss; pallor macrocytic anaemia; serum

protuberant; anal of skin and mucosa, proteins low, often hypo-
sphincter lax glossitis, aphthous kalaemia; faecal fat increased;
stomatitis X-ray of small bowel shows
'sprue' pattern; small bowel
biopsy - short, thick villi
tenderness or history of chronic alcohol- amylase and lipase elevated

fulness of epigast- ism common; glossitis, after acute attack; glucose
rium in some; weight loss tolerance test shows diabetic
ascites in some curve; faecal fat increased;
X-ray may show calcification
of pancreas
Abdominal weight loss or retarded sweat shows increased sodium

distension in growth; obstructive res- and chloride; faecal fat
infants; pro- piratory symptoms; cough, increased; chest X-ray-hyper-
lapse of rectum copious sputum; prostration inflation, often collapse of
from salt depletion in hot segment; small bowel X-ray -
weather, sweating increased nutritional deficiency pattern
liver may be weight loss and cachexia at tumour visible via proctoscope;
enlarged; tumour times; dull perineal ache in anaemia from blood loss;
often palpable on some; urinary frequency or leukocytosis at times; elevation
rectal digital tenesmus in some of SGOT and alkaline
phosphatase with hepatic
metastases
bowel is involved vomiting may not be marked and there is

constipation. The abdomen becomes distended and 'fluid
levels' are seen on X-ray.
(i) Paralytic ileus is an atony of the small intestine post-

operatively or complicating intestinal obstruction or
peritonitis. Secretions continue to be poured into the
intestine, which is unable to pass its contents onwards or to
absorb them. The patient becomes increasingly dehyd-
rated, with hypotension and collapse. Nasogastric suction
and intravenous fluids and antibiotics are required until
the causative condition is relieved or intestinal motility is
re-established.
U) Peritonitis may complicate any of these conditions. The

peritoneal membrane of the abdomen is similar to the
pleural membrane of the thorax. The visceral layer of
peritoneum covers the intestines and is not sensitive to
pain, the parietal layer lines the abdominal wall and is
pain-sensitive. The peritoneal cavity is the potential space
between the two layers. A large fold of peritoneum called
the greater omentum is spread like an apron over the
intestines, separating them from the anterior wall of the
abdomen.
Peritonitis is inflammation of the peritoneum and
results from spread of inflammation from abdominal or
pelvic organs.
Symptoms and signs:

pain;
tenderness and muscle guarding, which may remain
localized by the 'policeman' action of the greater
omentum, with subsequent healing or abscess form-
ation;
the peritonitis may become generalized with rapid pulse,
pyrexia and toxaemia from infection.
(k) Ascites. Ascites is the presence of fluid in the peritoneal

cavity.
Causes:
congestive cardiac failure - part of the generalized
oedema from fluid retention;
nephrotic syndrome (renal disease with albuminuria and
oedema);
cirrhosis of the liver - ascites due to low plasma albumin
and raised portal venous pressure, causing fluid
exudation into the peritoneal cavity.
malignant ascites - from peritoneal metastases in
carcinoma of the stomach, large intestine or ovary.
Symptoms and signs:
abdominal distension, but this is not marked in early
stages;
dullness to percussion over the flanks, the dullness shift-
ing when the patient is asked to role to one side;
increasing ascites will show the umbilicus becoming
everted and the abdomen tense and uncomfortable:
Diagnostic tap may be required in suspected malignant
ascites, a specimen of fluid being sent for cytology for
malignant cells. The fluid may be blood-stained and often
accumulates rapidly in such cases.
Chapter 6
The Digestive System (Liver,
Biliary Tract and Pancreas)
Disorders of the organs involved in the digestive system are in

general those that affect the adult, with the exception of
infective hepatitis in the young. Gallstones are commoner in
fertile females over 40 years of age than in men, cirrhosis of the
liver is of increasing frequency in the adult male of mature
years due to alcohol consumption. Pancreatic disease affects
both sexes equally.
(A) urine,
(B) blood tests,
(C) X-rays (including contrast media use and angiography),
(D) ultrasound scanning,
(E) biopsy.
Common symptoms of digestive organ disease will be:
(1) anorexia and nausea,
(2) jaundice,
(3) pain,
(4) fever,
(5) ascites (free fluid in the abdominal cavity).
93
(A) URINE TESTS

Bilirubin (pile pigment) gives a brown colour to the urine, and
on shaking in a test-tube, the froth is yellowish.
Reagent strips confirm presence of bilirubin.
Urobilinogen is colourless and reagent strips may be used.
Acetone may be detected by odour and confirmed by
reagent tablet or strip.
Sugar is detected by reagent strip test.
(B) BLOOD TESTS (e.g. liver function tests)

Test on venous blood include serum bilirubin, enzymes such as
SOPT (raised in liver cell dysfunction) and alkaline phos-
phatase (raised in obstructive jaundice), proteins and pro-
thrombin.
(C) X-RAY EXAMINATION

Cholecystography - the patient is given an evening dose of
iodine-containing substance excreted by the liver into the bile:
it becomes concentrated in a normal gallbladder, which will
show up on X-ray next morning. Further films after a fatty
meal will show contraction of a normal gallbladder and outline
the bile duct. Straight abdominal X-ray may in certain cases
show gallstones.
Percutaneous cholangiography - where X-ray contrast
medium injected into the liver allows demonstration of a
blocked biliary tree - may be of great help in localizing the site
of an obstruction.
Portal venography is also useful diagnostically in certain
particular diseases.
(D) ULTRASOUND SCANNING

This investigation shows abnormalities of the liver and biliary
tract including blockage from stones and the presence of
tumours. It is a non-invasive investigation, causing no
discomfort to the patient. It is becoming established as a most
useful early investigation in liver, gallbladder and pancreatic
disease.
THE DIGESTIVE SYSTEM 95
(E) LIVER BIOPSY
Using local anaesthetic, a special needle is inserted between the
right lower ribs in the mid-axillary line, and passed into the
liver from which a small specimen is withdrawn for micro-
scopical examination. This investigation is contraindicated if
the patient has a bleeding tendency or is severely jaundiced.
The liver, the largest organ in the body, is wedge-shaped, and

occupies the uppermost right part of the abdomen immed-
iately below the diaphragm, sheltered by the ribs. The portal
vein carries to it the food products absorbed in the intestine,
and it receives arterial blood from the hepatic artery.
The hepatic duct carries bile from the liver and joins the
cystic duct from the gallbladder to form the common bile duct.
This usually unites with the main pancreatic duct just before
opening into the second part of the duodenum. The gall-
bladder is a pear-shaped bag on the under-surface of the'liver,
opposite the anterior end of the ninth costal cartilage. It stores
and concentrates the bile.
Most of the liver cells are specialized hepatic cells, but the
liver also contains cells of the reticuloendothelial system. The
reticuloendothelial system includes cells in the spleen, liver,
lymph nodes and bone marrow. It has a scavenger function for
worn-out cells and foreign material, and a function in the
immunity mechanism, producing the immune globulins or
antibodies. Thus the liver may become involved in blood
diseases such as leukaemia and Hodgkin's disease.
FUNCTIONS OF THE LIVER

(1) METABOLISM AND STORAGE
Carbohydrates are metabolized and glucose stored as
glycogen. Proteins are synthesized from amino acids. Thus the
liver makes plasma-albumin and prothrombin, which is
necessary for blood coagulation; Vitamin K is required for its
synthesis. In protein breakdown, ammonia is formed and is
converted by the liver to urea which is excreted by the kidneys
in the urine.
Fats are catabolized to fatty acids which provide a reserve
source of energy when glucose metabolism is upset as in

diabetic ketosis. Vitamin D is partially hydroxylated and
stored in the liver, with vitamins A and B.
(2) DETOXIFICATION
. The liver renders harmless the body's waste products. It also
destroys toxic substances and drugs, or conjugates them
chemically to prevent their further action and allowing their
excretion in the urine or, in some cases, into the bile.
(3) BILE SECRETION
The liver produces the bile salts, which by their 'detergent'

action, cause the emulsification of dietary fats into small
globules for digestion by pancreatic lipase in the intestine. Bile
salts are necessary for the absorption of the fat-soluble
vitamins A, D and K. Bile also contains bile pigment, bilirubin,
which has no digestive function but gives bile its colour.
Bilirubin metabolism: the red blood cells become worn out
in 120 days, when they are taken up by cells of the reticulo-
endothelial system. The haemoglobin is broken down, iron is
detached from the haem and retained for further use; the
remainder of the haem molecule goes to form bilirubin. It is
carried by the bloodstream to the liver where it is taken up by
the hepatic cells.
Common Disorders of the Gastrointestinal

Organs
(1) JAUNDICE
Jaundice is a yellow discoloration of the tissues due to excess
bilirubin in the blood. Jaundice is often first noticed in the skin
of the abdomen, or in the sclera (white part) of the eyes, but an
observant nurse may note it in the plasma when reading an
ESR.
TYPES
(a) Pre-hepatic - excessive production of bilirubin
This is haemolytic jaundice or haemolytic anaemia, from

abnormal red-cell destruction (see Chapter 13, 'The blood and
lymphatic system').
There is no bile in the urine. This is because bilirubin is not
water-soluble when just formed from red cells. Because of the
large amount of bilirubin reaching the colon in haemolytic
jaundice, much urobilinogen is formed and reabsorbed, over-
whelming the excretory capacity of the liver, so that an excess
of urobilinogen appears in the urine.
(b) Hepatic
This is due to disordered function of the liver cells. It is caused

by infections, such as hepatitis, poisons such as carbon tetra-
chloride (used in dry-cleaning and as a fire extinguisher) and
benzene (a solvent), drugs and by some rare familial diseases.
Depending on the degree of swelling and obstruction to bile
outflow, the stools may be normal in colour or pale.
Reabsorption of bilirubin rendered water-soluble by passage
through the liver causes bile to appear in the urine. In the early
stages of liver cell dysfunction, the capacity of the liver to re-
excrete urobilinogen is one of the first functions to be
impaired. Urobilinogen is at this stage detectable in the urine.
(c) Post-hepatic or obstructive jaundice
This is due to blockage of the bile duct by a stone from the gall-
bladder, or by carcinoma of the head of the pancreas. The
jaundice is deep and the skin often itchy. The stools are pale
and clay-coloured, the urine dark brown from the presence of
bile pigment, bilirubin.
Effect
The bilirubin in the tissues is not in itself harmful in adults. In
haemolytic disease of the newborn (which is due to Rhesus
factor antibodies) the excess bilirubin is toxic to the infant
brain.
In obstructive jaundice fat digestion is impaired and vitamin

K cannot be absorbed. Prothrombin manufacture may also be
impaired by hepatic jaundice. Failure of blood coagulation
and bruising tendency results.
Drugs and the liver

If liver function is impaired drugs normally destroyed by the
liver may reach toxic concentrations in the bloodstream.
Morphine and barbiturates (excluding phenobarbitone which
is excreted unchanged in the urine) are such drugs and they
must not be given to patients suffering from disorders of the
liver.
(d) Jaundice due to drugs

The mechanisms of drug-induced jaundice are complex.
Substances such as carbon tetrachloride, chloroform, and
benzene are directly toxic, causing liver cell necrosis, and a
very high concentration of tetracycline and paracetamol may
have a similar effect. The anaesthetic halothane if used
repeatedly, and the monoamine oxidase inhibitors, used in
treatment of depressive illness, may cause a hepatitis-like
jaundice. Chlorpromazine and its derivatives, oral contra-
ceptives and sex hormones may cause a less severe sensitivity
(cholestatic) jaundice, which clears when the drug is stopped.
(2) VIRUS HEPATITIS - INFECTIOUS HEPATITIS AND

SERUM HEPATITIS
Cause
A virus present in the patient's stools and transmitted by faecal
contamination of food or water is the cause. Cases may occur
sporadically or in epidemics where hygiene is poor, and have
followed the eating of shellfish from sewage-polluted waters.
The incubation period is about 30 days. Jaundice is the
hallmark of the infection but may be mild, and many cases go
undiagnosed. The faeces are infective from about 2 weeks
before, to 2 weeks after, the onset of jaundice. Infectious
hepatitis is commonest in children and young adults.
Serum hepatitis is also a virus infection from blood or blood
products, infection is spread usually by blood transfusion or
by injection from contaminated syringes and needles. The
incubation period is up to 120 days. Adults are mainly
affected, the illness frequently being more severe than infect-
ious hepatitis.
The blood of some patients with serum hepatitis contains an
antigen related to the presence of a virus called the hepatitis-B
associated antigen, HbAg (or Australia antigen as it was first
found in the serum of an aborigine). It may persist for many
years due to a deficiency of the immunity mechanism and the
blood is infective, although the carrier may be symptomless.
This led to outbreaks of hepatitis in renal dialysis units. Though
screening for this antigen diminishes the risk, other viruses
may be responsible for cases of hepatitis: non-A, non-B
hepatitis.
Drug addicts are at risk from contaminated syringes, and as
hepatitis is common among homosexuals, secretions other
than blood transmit the infection. (e.g. saliva).
The virus is destroyed by autoclaving or dry heat steriliz-
ation but a better preventive measure is the use of disposable
equipment where possible, and the avoidance of blood
transfusion unless there is a clear indication for its use.
Gammaglobulin prophylaxis
Injections of this immune globulin may prevent the develop-
ment of infectious hepatitis after exposure in epidemics. This
measure is indicated in pregnant women. Gammaglobulin
prophylaxis is of less value in serum hepatitis.
Symptoms and signs

Loss of appetite.
Malaise and generalized aches.
Fever.
Nausea and vomiting occur.
Jaundice becomes manifest.
Abdominal discomfort with liver swelling and tenderness.
Fulminating cases develop deep jaundice and high fever and

may go into hepatic failure and coma.
The stools become pale during hepatitis.
The urine may contain excess urobilinogen in the earliest
stages, but with liver cell swelling and obstruction to bile
outflow this disappears and the urine becomes dark due to the
presence of bilirubin, which clears as the jaundice lessens.
Liver function tests in the blood are also abnormal.
Mental depression is often marked.
(3) CIRRHOSIS OF THE LIVER
Cirrhosis is diffuse fibrosis of the liver with areas of nodular

regeneration. (The word cirrhosis is derived from a Greek
word meaning tawny, the colour that the liver may acquire in
this condition.)
TYPES
There are two main types: portal cirrhosis and biliary cirrhosis.
Portal cirrhosis is the commoner type and is a disease of
middle-age. The patient is not usually jaundiced (except term-
inally), the trouble affecting the portal venous system, though
the liver cells are also involved.
Biliary cirrhosis is associated with obstruction to bile outflow,
which may be primary from intrahepatic disease or secondary
from extrahepatic biliary obstruction, and the patients are
jaundiced.
Primary biliary cirrhosis occurs in middle-aged women. The
cause is unknown; like chronic active hepatitis, it may be a
disturbance of immunity to hepatitis-associated antigen and
certain antibodies are detectable in the blood. There is
jaundice with dark urine and pale stools, and severe pruritus.
Secondary biliary cirrhosis occurs if bile duct obstruction from
stone, stricture, or carcinoma goes unrelieved for months or
years.
Portal cirrhosis
Causes
Alcoholism - the commonest cause in many countries.
Dietary deficiencies and effects of toxins and parasites
especially in the tropics.
Following virus hepatitis.

Right sided heart failure and constrictive pericarditis if
untreated.
Rare diseases with liver fibrosis - haemochromatosis from iron

deposition in pancreas and liver, and hepatolenticular degener-
ation (Wilson's disease) from copper deposits in the liver and
basal ganglia of the brain.
Symptoms and signs

Vague ill-health, anorexia and mild fever.
The finding of an enlarged liver and enlarged spleen. In portal
hypertension, distension occurs where veins of the portal
system anastomose with the systemic veins, causing varicose
veins at the lower end of the oesophagus, dilated vessels in the
abdominal wall near the umbilicus and splenic enlargement.
Haematemesis occurs from ruptured oesophageal varices,
though bleeding may occur from peptic ulcer or gastric
erosions commonly associated with alcoholism.
Anaemia is common.
Splenic enlargement may inhibit the release of cells from the
bone marrow (which remains active) resulting in deficiency of
platelets causing bleeding, and of white cells with increased
susceptibility to infections.
In liver cell dysfunction the appearance of vascular spiders on
the face, neck and arms may be seen. These are little red spots
consisting of a dilated arteriole from which tiny vessels radiate.
The skin of the palms of the hands is pink, contrasting with the
muddy colour of the skin as a whole in cirrhosis.
Ascites is common, from the combined effects of portal hyper-

tension and reduced serum albumin in the blood. (Albumin
normally maintains the osmotic pressure, the 'holding force'
by which fluid is retained in the circulation. The leakage of
fluid from the bloodstream to form ascites lowers the blood
volume, and compensatory mechanisms to retain fluid in the
body come into operation; these include secretion of the
adrenal cortical hormone aldosterone which causes salt and
water retention which further increases the ascites and causes
oedema.)
Aldosterone also causes potassium loss with muscle weakness
as a result.
Jaundice is a late sign, heralding liver cell failure, build-up of
toxic nitrogenous substances causes depression of brain
function or portal-systemic encephalopathy and coma.
The urine contains excess urobilinogen.
Liver function tests in the blood are abnormal, and the
electrolytes, especially potassium, must be checked.
Liver biopsy may elucidate the type of cirrhosis.
Barium swallow demonstrates oesophageal varices.
Portal venography may be helpful.
(4) LIVER CELL FAILURE AND HEPATIC COMA

Hepatic failure with jaundice, bleeding tendency and the ill
effects of increased circulating nitrogenous substances
absorbed from protein breakdown in the intestine, leads to
coma.
Causes
Acute liver poisoning and necrosis from chemicals such as
carbon tetrachloride, benzene and chloroform; and halo-
thane, paraquat, paracetamol poisoning and other toxins.
Fulminating virus hepatitis.
Cirrhosis of the liver. Precipitating factors include alcohol
intake, intercurrent infections, gastrointestinal haemorrhage
causing excessive protein load, and potassium deficiency.
Symptoms and signs

These are those of the causative condition, of which the
commonest is:
Cirrhosis.
Increasing jaundice.
Fever and effects of the nitrogenous toxins.
There is a flapping tremor of the outstretched hands, lethargy
and variable mental confusion.
The electroencephalogram (EEG) shows typical changes in the
brain waves.
(5) SECONDARY CARCINOMA
The liver is a very common site of metastatic growths, spread

by the portal or systemic veins from primary carcinomas in the
abdomen, such as stomach and large intestine, or in the chest,
such as carcinoma of the lung or breast.
Symptoms and signs

There may be evidence of the primary growth, but the
secondary carcinoma in the liver may present first.
There is malaise, lassitude.

Weight loss.
Abdominal swelling: The liver may be huge and nodular.
Ascites from peritoneal metastases.
Jaundice may be mild or severe when major bile ducts are
invaded.
The urine may contain bilirubin and/or urobilinogen.
(6) GALLSTONES AND THE BILIARY TRACT

Gallstones are formed when some of the constituents of the
bile are deposited from solution. There may be excessive
production of cholesterol by the liver. As bile is concentrated
in the gallbladder, stones are most frequently formed here.
Gallstones occur at all ages, but are very common in middle-
aged women who are obese and have borne many children -
women who are fair, fat, fertile and forty. Hormonal effects
on bile composition or gallbladder motility, and infection
may be causative factors.
Symptoms and signs

May be symptomless, especially in the elderly.
Associated with cholecystitis.
Bile duct obstruction with colic, jaundice and cholangitis from
infection of the stagnant bile.
(7) CHOLECYSTITIS
(a) ACUTE
This is acute inflammation of the gallbladder, usually
associated with a gallstone obstructing the neck of the gall-
bladder or the cystic duct, and there is super-added infection
often with Escherichia coli.
Symptoms and signs

Precipitated by a fatty or heavy meal.
Epigastric discomfort followed by severe pain and tenderness
at the right upper quadrant over the gallbladder as the
peritoneum becomes involved.
Pain may be referred to the right scapula or tip of the shoulder.
Anorexia, malaise and fever.
Occasionally vomiting but jaundice suggests bile duct obstruc-
tion.
The white cell count is raised.
Straight X-ray may show opaque stones.
(b) CHRONIC
This presents as recurrent attacks of acute cholecystitis, or as
dyspepsia and upper abdominal discomfort often provoked by
fatty foods or a heavy meal.
Thus the diagnosis of chronic cholecystitis must be
confirmed by cholecystography, which shows gallstones and a
poorly functioning gallbladder.
(8) BILE DUCT OBSTRUCTION

This is caused by a gallstone passing into the common bile
duct, resulting in biliary colic, jaundice and cholangitis.
Symptoms and signs

Biliary colic is severe intermittent colicky pain or a more
prolonged pain building up over an hour or two, felt in the
epigastrium or right upper quadrant of the abdomen, and
accompanied by vomiting.
Jaundice may be mild or deep and is obstructive in type with
pale stools and dark urine, but the obstruction is rarely
complete so that the stool colour may vary from day to day.
Cholangitis is inflammation of the bile duct from infection of
the stagnant bile.
This causes fever, often of an intermittent type, accompanied
by pain and jaundice.
These include blood culture, ultrasonic scan and cholangio-
graphy.
THE PANCREAS
The pancreas is an elongated gland that lies across the upper
part of the posterior wall of the abdomen, its head in the loop
of the duodenum, its body and tail extending to the left behind
the stomach.
The gland cells secrete the pancreatic juice containing
enzymes which act on protein, fat and carbohydrate. These
enzymes are activated on meeting the duodenal juices. The

main duct of the pancreas unites with the bile duct to form
what is called the ampulla just before entering the second part
of the duodenum. The sphincter surrounds the ampulla and
prevents reflux of duodenal contents into the pancreatic duct.
The islet cells, or islets of Langerhans, secrete the hormone
insulin into the bloodstream. Insulin is especially concerned
with glucose metabolism, and deficiency of its action results in
diabetes mellitus.
(9) PANCREATITIS
(a) ACUTE
Associated with disease of the biliary tract or gallstones - with
alcoholism - reflux of duodenal contents into the pancreatic
duct activates the enzymes resulting in self-digestion of the
pancreas and necrosis of surrounding fat - an acute inflam-
matory process.
Symptoms and signs

Sudden agonizing upper abdominal pain.
Nausea and vomiting.
The abdomen is tender and rigid.
Pallor, rapid pulse and often hypotension and collapse.
Shock due to lowered blood volume from outpouring of fluid
into the intestine.
The diagnosis of acute pancreatis is confirmed by a very high
serum amylase, one of the enzymes that leaks into the blood-
stream.
(b) CHRONIC
In chronic pancreatitis there is a gradual destruction of the
pancreatic cells with replacement fibrosis and permanent
impairment of function.
12X
,
, 20.5X
,
,,
11 X
10X
I
9X
ax
7X
,
I
I
Serum Amylase
6X I Serum Lipase
5X
,,
I Urine Amylase
4X
3X
/
2X
/
Normal ,
Day I 3 5 7 9 11 13 15 17
Amylase and lipase elevations in acute pancreatitis
Cause
The cause is often unknown, but alcoholism and dietary
deficiencies may be responsible.
Sequel to acute pancreatitis or biliary tract disease.
A gallstone pressing on the pancreatic duct.
Carcinoma of the pancreas may also be associated.
DIFFERENTIAL DIAGNOSIS OF ABDOMINAL PAIN-

Character Location Produced or
relieved by
Peptic ulcer gnawing, aching in upper precipitated by

epigastrium, spicy or greasy
may radiate to food, anxiety;
back usually relieved
by antacids or food;
at times by vomiting
Perforated initially severe, at first epigastric, initial pain

peptic ulcer continuous; then then generalized; spontaneous, later
less severe but may radiate to top pain made much
still continuous of one or both worse by movement
shoulders
Intestinal intermittent, epigastric and onset spontaneous

obstruction, colicky, persistent periumbilical; and unpredictable
small bowel with distension or localized over
strangulation strangulation
when present
Intussusception sudden onset, maximal in vomiting may give

severe, inter- periumbilical give temporary
mittent - lasts a region relief
few minutes,
recurs after
minutes or hours
Intestinal onset sudden; usually onset

obstruction, colicky, each hypogastric, spontaneous
large bowel spasm less than a in midline
minute, comes at
intervals of a few
minutes
Due to Gastrointestinal Disorders
physical findings and symptoms findings
abdomen soft, but nausea and vomiting may have iron deficiency
may show diffuse common, appetite good - anaemia, blood in stool;
epigastric tender- weight stable; retrosternal X-ray after barium will show
ness burning and increased ulcer crater
salivation may occur; sour
taste in mouth frequent;
abdominal cramping on left
side common - from
associated irritable colon
abdomen initially preceding ulcer symptoms chest X-ray may show free air
diffusely rigid, usually present; pale, under diaphragm; leukocytosis
then tender; with sweating, weak pulse, present
peritonitis, shallow respiration -
rigidity goes, but initially retching; hiccups
still tender,
becomes distended
abdomen soft weak, shock, no fever until X-ray of abdomen - fluid

until distension strangulation; vomiting - levels in 3-4 h
develops then most prominent with high
generalized tender- obstruction; constipation,
ness visible peri- dehydration and oliguria
stalsis of stomach
or small bowel -
loud bowel sounds,
borborygmi -
rebound
tenderness
a sausage- usually one normal stool barium enema: one portion

shaped mass may after onset, then bloody of bowel invaginated into
be palpated in mucus and constipation; another
the abdomen - vomiting late
becomes firmer
with pain; the
right iliac fossa
feels empty; signs
of obstruction
distension early vomiting may not be present, X-ray of abdomen - fluid

and marked; but nausea is; constipation, levels in 3-4 h
increased no flatus
peristaltic
sounds, more
marked during
pain
(continued overleaf)
DIFFERENTIAL DIAGNOSIS OF ABDOMINAL PAIN -

relieved by
Appendicitis initial colicky colicky pain made worse by

pain in many, then in central extension of right
persistent and abdominal area, thigh
continuous, of continuous in
varying intensity right iliac fossa
Pancreatitis severe, epigastric; may accompany

continuous, may radiates widely, mumps or follow
last days to week often to back and/ laparotomy;
or one or both recurrent type
loins; or to left often follows
scapular region alcoholic excess
Cholecystitis continuous - right upper worsened by

varies from mild quadrant and breathing
to severe- epigastrium; may
present before be referred to
nausea and right hypochond-
vomiting rium and tip of
right shoulder
Biliary colic severe pain - maximal in right slightly

crescendo for upper quandrant relieved by
20 min then or epigastrium, flexed
gradually recedes may radiate to posture
right shoulder
Diverticulitis acute, initially may be

continuous, may hypogastric, then precipitated
last several days; then maximal in by large meals with
collicky pain, as left iliac fossa; much roughage or
well, at times, may radiate to by strenuous
from partial low back exercise
obstruction
Due to Gastrointestinal Disorders (cont'd)
tenderness - often anorexia, indigestion leukocytosis always present

often rebound and flatulence; diarrhoea
rigidity; super- precedes attack at times;
ficial hyper- some nausea and vomiting,
aesthesia; audible but not persistent; fever and
borborygmi rapid heart rate; urinary
frequency, tenesmus and
rectal tenderness
abdomen usually retching - at times marked leukocytosis; serum

tender in lower incessant - often bilious amylase over 500 initially,
epigastrium; vomiting; fever; icterus at may fall during attack; serum
either somewhat times; in severe cases - shock Ca ++ may be reduced; X-ray -
rigid or soft; with cold, clammy skin - pancreas calcified in recurrent
marked rigidity is often purpuric staining of type
rare left flank and/ or perium-
bilical region after several
days
always local often history of biliary leukocytosis always present;

tenderness in disease and fatty food plain film of abdomen may
right upper intolerance; vomiting slight show stone - cholecysto-
quadrant; often unless stones or peritonitis; gram will usually show non-
local rigidity usually constipated; some functioning gallbladder
fever, more with cholangitis;
usually no jaundice
abdomen is often history of biliary radio-opaque stones may be

soft - there may disease or colic; much seen on flat film of abdomen;
be deep local nausea and vomiting - if no filling of gallbladder on
tenderness in bilious with retching, intravenous cholangiogram,
right upper belching, cold sweat - suspect blocked cystic duct
quadrant patient appears near (or severe liver disease);
collapse; diarrhoea at times, cholangiogram may show
fever and chills with dilated common duct and
cholangitis; jaundice in some location of stone(s)
guarding and long history of constipation, leukocytosis usual; barium

local rigidity in with diarrhoea at times; enema X-ray shows diver-
left lower flatulence; prior rectal ticula - irregular narrowing,
quadrant - vague bleeding or bloody stools in wedge-shaped defects suggest
mass may be most; nausea and vomiting; diverticulitis
palpable fever and tachycardia -
may have rectal tenderness
DIFFERENTIAL DIAGNOSIS OF ABDOMINAL PAIN -

relieved by
Ulcerative usually maximal in often

colitis intermittent, hypogastrium or precipitated by
colicky; left lower emotional stress;
continuous with quadrant often relieved by
acute dilatation or defaecation
perforation
DIFFERENTIAL DIAGNOSIS OF ASCITES-

Time and Amount of
speed of onset fluid
Portal cirrhosis gradual onset, but may be often massive

sudden; early in course
Post-necrotic cirrhosis gradual onset; any time in variable, usually less

course than portal cirrhosis
Acute alcoholic hepatitis gradual or sudden onset; variable, may be massive

usually early in course
Portal vein thrombosis sudden onset; usually large to massive

early in course
Metastatic malignant gradual onset; usually variable; rarely massive

liver disease early in course
Due to Gastrointestinal Disorders (cont'd)
abdomen usually diarrhoea frequently WBC count normal, many

soft, not tender - nocturnal, often bloody toxic forms; alkalosis with low
distended, tender with muco-pus; tenesmus, Na +, K +, Cl- and protein;
with acute fever, malaise; rectal - tight proctosigmoidoscopy -
dilatation sphincter hyperaemia, granularity,
purulent exudate, ulceration;
barium enema - ragged out-
line, ulceration, narrowing,
shortening, loss of haustration
Due to Hepatic Diseases

Other associated signs and Key laboratory findings
symptoms
weakness, fatigue, jaundice; right liver function tests show non-specific abnor-
upper quadrant abdominal pain; malities; occasionally hyper lipaemia with or
gynaecomastia without anaemia; diagnostic test - liver biopsy
weakness, fatigue, jaundice; often liver function tests often non-specifically

gynaecomastia and loss of libido; . abnormal; occasional abnormal serologic tests,
upper gastrointestinal bleeding LE phenomenon, hypergammaglobulinaemia;
may occur; palmar erythema, liver biopsy diagnostic
oedema
jaundice, fever, abdominal pain, liver function tests non-specifically and

dehydration; occasionally haem- moderately abnormal; uric acid up, potassium
atemesis; palmar erythema down; occasional hyperlipaemia, anaemia which
may be haemolytic
right upper quadrant abdominal liver function tests variable; occasional

pain; often nausea, vomiting, pancytopenia or isolated cytopenia;
haematemesis, melaena in over diagnostic test - splenoportography
50%; oesophageal varices in
more than 90%
cachexia - weakness, anorexia, liver function tests - elevated alkaline

fever; right upper quadrant phosphatase, SOOT; bilirubin sometimes high;
abdominal pain; jaundice in often anaemia and leukocytosis; liver scan
some; occasional upper gastro- shows space-occupying lesion; liver biopsy
intestinal bleeding usually diagnostic
Symptoms and signs

Bouts of upper abdominal pain, persistent and demoralizing,
often precipitated by a heavy meal or alcohol.
Pain may be worse lying flat.
Slight jaundice, and fever.
Sometimes there is no pain, the condition presenting as
pancreatic insufficiency with malabsorption syndrome from
lack of digestive enzymes.
There is weight loss and steatorrhoea - loose, pale, offensive,
fatty stools.
Diabetes in the late stages, from destruction of the insulin-
secreting islet cells. There is polyuria and thirst.
Straight X-ray may show pancreatic calcification.
The serum amylase may be slightly raised.
Stools show a high fat content (normally less than 6 g/24 h).
Glucose tolerance test may show a high diabetic curve instead
of the flat curve of intestinal causes of malabsorption, and
xylose absorption is normal.
Ultrasonic and radioisotope scans prove helpful.
(10) CARCINOMA OF THE PANCREAS

This occurs in the middle-aged and elderly.
Symptoms and signs

The onset is insidious.
Upper abdominal pain similar to that in chronic pancreatitis.
Anorexia and weight loss.
Obstructive jaundice may be the first sign.
The jaundice is deep with itchy skin, pale stools and dark
urine.
Metastases are frequently the first clinical indication - ascites
from peritoneal deposits, or liver swelling.
Involvement of the inferior vena cava causes venous
obstruction and oedema.
Barium meal may show distortion of the loop of the
duodenum. The ESR may be raised, as in any malignant
disease.
Ultrasonic and radioisotope scanning of the pancreas may be
helpful.
Chapter 7
The Urinary System
The commonest disorder of the urinary system is acute

infection. In primary care infection will be the most frequent
cause of consultation for disorders of this system, but only 5070
of hospital admissions will be due to disorders of the urinary
system. Renal calculi, renal colic, nephritis, and renal failure
will be the most frequent causes of hospital admission for
diseases of this system, but they account for less than 1070 of all
deaths.
(A) urine,
(B) blood and urine tests to determine renal function,
(C) X-rays (plain and contrast),
(D) cystoscopy,
(E) Renal biopsy.

(1) dysuria and/or frequency,
(2) haematuria,
(3) pain,
117
(4) oedema,
(5) hypertension.
(A) EXAMINATION OF THE URINE

Appearance
Colour
The normal yellow or amber colour is due to urochrome. Dark
urine may simply be concentrated urine or due to the presence
of bile (bilirubin). Blood in the urine, haematuria, is either
frank and obvious or causes a dark, 'smokey' urine.
Deposits
Urates form a brown or pink deposit when urine cools on
standing. Phosphates are white and appear in neutral or
alkaline urine. A cloud of mucus may be seen. These are
normal findings and should be distinguished from pus in the
urine, pyuria (which may be creamy and offensive) and from
haematuria, but microscopic examination may be necessary.
Volume and specific gravity
The volume varies from 500 to 3000 ml124 h, average 1500 ml,
and depends on the· fluid intake and water vapour losses
through the skin. Polyuria is an increased output of urine,
oliguria a diminished output, and anuria complete suppression
of urine. The urine volume must be carefully charted
weighing the patient daily gives a further check of output.
Reaction (acidity)
This is tested by pH indicator paper strip. Urine is normally

slightly acid, pH 6. The pH may drop to 4 if metabolism is
increased, or in states of acidosis. Ingestion of alkalis and
fruits renders the urine alkaline, pH above 7.
Presence of sugar
Glucose is present in the urine in diabetes mellitus, and in
patients with a low renal threshold for glucose reabsorption.
THE URINARY SYSTEM 119
Acetone - ketoacids
Ketonuria occurs on severe vomiting, starvation, and diabetic
ketosis and coma. It is detected by strip test or tablet.
Protein
Proteinuria is persistent and often heavy in the nephrotic
syndrome. It occurs in acute nephritis, hypertensive kidney
disease and in chronic renal failure. In urinary tract infections,
pus in the urine may cause slight proteinuria but this is not a
reliable index of such infection.
Proteinuria may occur in high fever and cardiac failure. In
toxaemia of pregnancy there is hypertension, oedema and
proteinuria.
Strenuous exercise may cause proteinuria, and in some
people it follows prolonged standing, but is absent in a
specimen tested after a period of recumbency.
In all these conditions the protein present is albumin, which
has a small molecule so that it escapes through the glomeruli.
Bilirubin and urobilinogen

These may be found in the urine in diseases of the liver and
biliary tract.
Blood - haematuria
Blood in the urine is called haematuria. If arising from the
kidneys the blood will be intimately mixed with the urine. If
from the prostate or urethra, blood may only be present at the
start of micturition. Painless haematuria most commonly
arises in the bladder or prostate, but a renal lesion may be
responsible.
Causes
(1) Systemic: blood disorders such as purpura; anticoagulant
overdosage.
(2) Renal: acute glomerulonephritis;
renal infarction from arterial thrombosis or
embolism;
hypernephroma (carcinoma) - this is painless,

there may be a palpable mass;
polycystic disease of the kidneys;
trauma.
(3) Ureteric: stones - usually associated 'renal colic'.
(4) Bladder: papilloma and carcinoma;
schistosomiasis, a parasitic infection.
(5) Prostate: carcinoma.

(6) Urethra: caruncle, and trauma.
A large amount of blood is obvious, lesser quantities give the

urine a 'smokey' appearance, or the amount may be so small
that microscopical examination is necessary to detect the red
cells.
Microscopical examination
This allows the detection of red cells, pus cells (pyuria) and
casts. Casts are formed in the renal tubules, and the presence
of cellular casts indicates active renal disease.
Specimens for bacteriology

Midstream urine (MSU). A catch specimen in midstream is
taken into a sterile wide-mouthed container (preliminary
cleansing of the labia in the female with sterile water may be
advisable).
The specimen should reach the laboratory within 1 h. The
number of colonies of organisms grown, the colony count, is a
better index of urinary tract infection than the amount of pus
cells present, a colony count of over 100 OOO/mi urine being
significant.
Cytology: an early morning specimen is examined for

malignant cells in patients with suspected carcinoma of the
urinary tract, especially bladder carcinoma.
(B) BLOOD AND URINE TESTS TO DETERMINE RENAL
FUNCTION
Blood urea
The normal blood urea is 2.5-7.5 mmolil (15-45 mg/dl). The
level is raised in renal failure and the rate of rise is more
important than the absolute level.
Other routine blood tests include the serum electrolytes
sodium, potassium and chloride, acid-base measurements
such as pH and bicarbonate, and estimation of calcium and
phosphorus.
Clearance tests
The amount of a substance cleared from the plasma by the
kidney's filter can be estimated by measuring its plasma
concentration, and its urine concentration over a set time. A
substance can be injected intravenously for this test, or altern-
atively one of the substances already present in the plasma can
be utilized - urea or creatinine. Thus the creatinine clearance
test (estimated on a 6-24 h urine collection) is used clinically as
a measure of the glomerular filtration rate and is normally
120mlimin.
Urine concentration test

The patient is given no fluids after 6 p.m.; the bladder is
emptied at 10 p.m. The following morning, the urine specific
gravity should be 1022 or higher. The concentrating power of
the kidney becomes impaired in disease such as chronic renal
failure; the specific gravity being fixed at 1010.
The specific gravity parallels the urea concentration, a
healthy kidney being able to produce a urinary area of at least
2g/100ml.
(C) X-RAYS
Plain X-ray may show the kidneys, and any opaque stones. In
intravenous pyelography (lVP) radio-opaque substance is
injected into a forearm vein. It is excreted by the kidneys,
demonstrating their size and function, and showing also the

renal pelvis, ureters and bladder.
Arteriography
A radio-opaque medium is injected into the aorta near the
renal arteries by direct puncture through the lumbar region, or
through a catheter inserted from below via the femoral artery.
This demonstrates the renal arteries and circulation.
(0) CYSTOSCOPY
This is the examination of the bladder through an instrument
passed by the urethra under general anaesthetic. Catheters can
be passed into the ureters and a radio-opaque medium allows
'retrograde pyelography'.
(E) RENAL BIOPSY

A specimen of kidney tissue is obtained by a needle inserted
through the lumbar region using local anaesthesia. The biopsy
is examined by ordinary and electron microscopy. The
procedure is contraindicated in bleeding disease and severe
uraemia, and carries a risk of causing a renal haematoma.
Common Disorders of the Urinary Tract

(1) URINARY TRACT INFECTION
Cause
Urinary tract infection occurs from bacterial invasion.
(a) Cystitis (inflammation of the bladder) from bacterial
infection is very common in women, the short urethra in
the female allowing entry of bacteria such as Escherichia
coli (the bowel organism).
(b) Acute pyelonephritis
Symptoms and signs
frequency, pain or burning on micturition;
there may be tenderness over the bladder;
pain and tenderness at one or both loins;
rigors and fever;
vomiting is common in children.
(c) Chronic pyelonephritis
This may present as recurrent attacks of acute pyelo-
nephritis and loin aches, or there may be symptomless
bacteriuria.
(d) Tuberculosis of the urinary tract
This was a complication of pulmonary tuberculosis and
may still be seen in patients whose drug therapy was non-
existent or inadequate, from a lurking focus of infection.
The kidneys and bladder are involved; symptoms are those
of pyelonephritis and there may be haematuria.
(2) URINARY TRACT STONES (CALCULI)

Symptoms and signs
Renal colic is really ureteric colic from the passage of a stone,
which tends to become impacted at the lower end of the ureter.
Pain at the loin, radiating to the groin, building up to
maximum severity over about \12 h, then declining only to
recur or disappear if the stone is passed into the bladder.
Haematuria may occur.
The stone may eventually pass out through the urethra.
Complications include stasis and infection.
Obstruction may have a back-pressure effect on the kidney,
causing hydronephrosis, a dilatation of the renal pelvis, which
if infected becomes a pus-containing pyonephrosis.
Renal function becomes impaired.
(3) ACUTE GLOMERULONEPHRITIS (TYPE 1

NEPHRITIS)
This is commonest in children, especially the undernourished,
but may occur in adults.
Causes
The commonest cause is an antecedent throat infection with
certain strain of haemolytic streptococci. It is an allergic
response in both kidneys about 10 days after such infection.
Antigen-antibody immune complexes are formed and
produce an inflammatory, cellular reaction at the capillaries of
the renal glomeruli.
Other disease involving small blood vessels may be causative
- anaphylactoid (Henoch-Schonlein) and other purpuras,
systemic lupus erythematosus and polyarteritis nodosa.
Symptoms and signs

Oedema, especially of the face, giving a pale, puffy appear-
ance.
Urine is initially diminished in amount.
Haematuria.
Onset is usually abrupt (but there may be history of sore
throat).
Malaise.
Shivering, fever.
Aches at the loins.
Blood pressure is slightly raised.
InveStigations
Urine contains red cells and casts, is of high specific gravity
and may contain protein.
Throat swab and anti-streptolysin 0 (ASO) titre may confirm
antecedent streptococcal infection. The ESR is raised.
Important nursing observations include pulse and temperature
chart, blood pressure, daily urine volumes and daily weighing
of the patient.
Severe hypertension, persistent proteinuria or rising blood
urea occurs in adult acute nephritis; such cases merge into
nephrotic syndrome or renal failure.
(4) NEPHROTIC SYNDROME
Causes
Subacute glomerulonephritis (Type 2 nephritis). This is
responsible for about 75!r!o of the cases. The cause is unknown
but cases may follow an episode of acute glomerulonephritis.
It is an immune-complex disease.
Renal vein thrombosis.
Systemic disease affecting the kidneys - amyloid disease,
systemic lupus erythematosus, diabetes, malaria, subacute
bacterial endocarditis.
Poisons and drugs.
In all these disorders the renal glomeruli have become
abnormally porous, leaking out albumin into the urine. The
plasma albumin level therefore falls. Albumin in the plasma
maintains the osmotic force which attracts water into the
circulation. The fall in the plasma albumin results in water
passing from the circulation into the tissues, causing oedema.
The tendency for the circulating blood volume to fall causes
excess aldosterone secretion, with salt and water retention,
worsening the tissue oedema.
Symptoms and signs
The first complaint is often ankle swelling, then oedema
spreads to the legs, body and face which is pale and puffy.
There may be ascites, and pleural effusion.
There need be no urinary symptoms; perhaps some frothing at
micturition due to the albumin in the urine.
Due to the protein loss, which includes some antibodies,
resistance is lowered and patients are prone to infection, such
as respiratory tract infections.
The course is variable and proteinuria may diminish as diseased
nephrons are destroyed but total renal function deteriorates,
the patient passing into renal failure.
Investigations
Urine contains 5 g or more albumin per 24 h, but initially is of
normal specific gravity. The plasma albumin is low, and the

cholesterol high. Blood urea and electrolytes are initially
normal.
Renal biopsy may be necessary.
Nursing observations include blood pressure, urine volume
and daily weighing of the patient.
(5) RENAL FAILURE

(A) ACUTE RENAL FAILURE
Causes
(1) Pre-renal-lack of blood supply to the kidneys:
(a) haemorrhage - injury, haematemesis;
(b) fluid loss from vomiting, diarrhoea or severe burns;
(c) prolonged hypotension from cardiac failure, or septi-
caemia.
(2) Renal:
(a) some cases of acute nephritis:
(b) renal cortical necrosis in pregnancy, and the renal
damage that may complicate operations in jaundiced
patients;
(c) mis-matched blood transfusion, and following crush
injuries causing sludging of blood and nephron
damage;
(d) poisoning by overdose of certain drugs.
(3) Post-renal: obstruction in the ureters, bladder or prostate,
such as stones, carcinoma, or fibrosis.
Symptoms and signs

There is diminished output of urine.
A history suggestive of renal disease such as polyuria, or
anaemia, and the event may have been precipitated by an
infection or lowered fluid intake.
Acute uraemia - drowsiness, twitching and vomiting.
(S) CHRONIC RENAL FAILURE - URAEMIA
Chronic renal failure is a disorder of gradual onset, the end
result of many chronic diseases of the kidneys. Biochemical
evidence of deteriorating renal function, such as a rising blood
urea precedes the clinical picture, for symptoms do not appear
until 75!t!o of the renal function has been destroyed.
Causes
Chronic glomerulonephritis.
Chronic pyelonephritis.
Hypertensive kidney disease.
Chronic urinary tract obstruction (stones, enlarged prostate).
Less common causes are amyloid disease, systemic lupus
erythematosus, gout, diabetes and polycystic disease of the
kidneys.
The kidneys are small and scarred. Most of the nephrons have
been destroyed, and there is a lack of sufficient numbers to
excrete the body's waste products and to control fluid, electro-
lyte and acid-base balance.
Uraemia, a high blood urea, is the hallmark of renal failure.
Urea is itself non-toxic, but it is the toxic end-products of
protein metabolism, plus the systemic effects of the disordered
renal function, that cause the symptoms.
Symptoms and signs

Chronic renal failure occurs in middle age, men being more
commonly affected (from the effects of hypertension).
Malaise, lack of energy.
Anaemia.
Raised blood pressure.
Polyuria.
Any system may gradually become affected:
DIFFERENTIAL DIAGNOSIS OF PAIN ON URINATION

Onset Course Type of Other urinary
pain symptoms
Acute acute may become usually frequency; urgency;

urethritis chronic burning terminal haematuria
during may occur
urination
Calculus - acute spontaneous sharp - in sudden interruption

bladder or passage may glans penis or of urinary stream may
urethral occur radiating down occur; commonly
penis; burning frequency and
if infection urgency; terminal
present haematuria
Bladder usually variable sharp or gross haematuria; with

tumours insidious burning, most infection - urgency,
commonly at frequency, nocturia;
termination of hesitancy, diminished
urination stream in some
Acute cystitis acute usually character- frequency; nocturia;

prompt istically urge, incontinence;
resolution terminal haematuria
with therapy burning
Tuberculosis insidious chronic, usually frequency; nocturia;

of the urinary progressive terminal haematuria
tract
Associated signs and symptoms Other laboratory findings
urethral discharge; itching or burning Trichomonads, rods, cocci may be found

in urethra; redness of urethral meatus in discharge; bacteria, WBCs in initial
portion of urine; cultures may isolate
bacteria
often urethral discharge, palpable mass; urinalysis - protein, RBCs, WBCs,

dull aching or sharp pain increased by bacteria; plain film, excretory urograms
movement with bladder calculus or cystoscopy for locating calculus
pelvic mass may be palpable; weakness, anaemia; urinalysis - frequently RBCs

weight loss, uraemia may develop WBCs, bacteria; tumour cells may be
found on exfoliative cytology; cystogram,
cystoscopic examination may be
diagnostic
dull suprapubic discomfort; cloudy leukocytosis; urinalysis - pus cells,

urine; occasionally tenderness over bacteria, occasionally RBCs
bladder; pyelonephritis or prostatitis
may accompany
malaise, fatiguability, fever, night anaemia; positive tuberculin test; pyuria;

sweats; suprapubic pain; chronic urine cultures often positive for M. tuber-
cystitis; thickened epididymis culosis; chest X-ray may show evidence
of tuberculosis; X-rays or urograms may
show characteristic lesions
DIFFERENTIAL DIAGNOSIS OF HAEMATURIA

Onset Character Pain on Course
urination
Cystitis usually usually dysuria usually self-limited;

acute terminal, common may become chronic
may be total
Benign usually initial, usually benign, frequently

papilloma of acute terminal, painless recurrent
the bladder or total
Urethritis usually usually often prolonged

acute initial, may dysuria
be terminal
Acute acute total painless variable

glomerulone-
phritis
Chronic insidious total painless usuaily progressive -

glomerulone- eventual renal
phritis failure
Trauma to the usually initial, painless or self-limited or

urinary tract acute terminal, painful rapidly fatal
or total
Acute pyelone- acute total dysuria usually self-limited

phritis common
Nephritis acute total usually usually benign;

painless frequent recurrent
attacks with
persistence of
haematuria
frequency, low back pain, urgency, pyuria; bacteriuria; proteinuria;

lower abdominal pain, lassitude, low- cystoscopy may show congested mucosa
grade fever; sometimes nausea, with numerous bleeding points
vomiting, signs of sepsis; cloudy urine;
suprapubic tenderness
usually no accompanying signs or cystoscopy often shows papilloma;

symptoms; rarely frequency, urgency, excretory urography may show mass
dysuria; occasionally urinary obstruc-
tion in females
often urethral discharge, inflammation urine may contain bacteria or WBCs;

of urethral mucosa; sometimes bacterial culture of urethral discharge
frequency, urgency positive in 20070
typically, preceding pharyngitis; usually often proteinuria; urine sediment shows

weakness, anorexia; often periorbital red blood cells, granular, and epithelial
oedema; sometimes shortness of breath, cell casts
hypertension, headache, convulsions;
often signs of congestive heart failure;
often abdominal pain, nausea, and
vomiting; usually scanty urine
sometimes nephrotic syndrome - heavy serum creatinine often elevated; urine

proteinuria, hypoalbuminaemia, sediment may show red blood cells, white
oedema; may progress to signs of renal blood cells, granular and cellular casts
failure - fatigue, breathlessness,
nocturia, nausea, hiccups, pericarditis,
pleurisy, insomnia
with renal injury - abdominal pain and intravenous pyelography may be

tenderness, fulness in loin; with ureteral diagnostic
injury - flank pain, oliguria, fever,
azotaemia; with bladder injury - shock
and haemorrhage, lower abdominal
pain and tenderness, sometimes
peritonitis; with urethral injury - pain
and extravasation of blood in perineum
fever, shaking chills, flank pain; leukocytosis; urine sediment shows many
often nausea, vomiting; usually WBCs, WBC casts, RBCs and bacteria;
tenderness in kidney region positive urine culture; sometimes
positive blood culture
febrile illness or sore throat; hyper- urine sediment may show red cells,
tension may occur; occasionally joint granular, and hyaline casts, proteinuria;
pain; rarely renal failure, oedema renal biopsy shows focal areas of
glomerular involvement
DIFFERENTIAL DIAGNOSIS OF HAEMATURIA (cont'd)

Onset Character Pain on Course
urination
Renal calculi usually total painful when usually self-limited,

acute renal colic often recurrent
present
Carcinoma of usually frequently painless unless progressive

the bladder insidious terminal passage of
clots causes
obstruction
renal colic common; often frequency, X-rays may demonstrate stones; urine
vomiting; sometimes tachycardia, sediment may show bacteria or crystals;
hypotension, often tenderness in renal sometimes abnormal serum calcium,
area phosphorus, uric acid, alkaline
phosphatase
often associated urinary tract cystogram may demonstrate urethral

infection; uraemia, anaemia, weight obstruction, filling defect of bladder
loss in advanced cases; pelvic mass or flattening of bladder wall;
may be palpable cystoscopy will visualize tumour
DIFFERENTIAL DIAGNOSIS OF OLIGURIA AND ANURIA

Oliguria and/ Onset Course
or anuria
Dehydration oliguria insidious reversible with

more common or acute correction of
dehydration
Congestive usually acute or reversible with

heart failure oliguria, insidious correction of CHF
rarely anuria
Acute oliguria acute usually recovery in

glomerulone- more common 1-2 weeks, occasionally
phritis irreversible renal failure
Acute toxaemia oliguria in insidious or usually recovery with

of pregnancy severe pre- acute termination of pregnancy
eclampsia,
anuria in
eclampsia
Multiple anuria or acute onset usually fatal outcome

myeloma oliguria
Renal failure - oliguria insidious fatal progression unless

end-stage chronic progressing dialysis or transplant
renal disease to anuria
thirst, fever; lassitude; tachycardia, often ECG abnormalities; serum hyper-

postural hypotension common; dryness tonicity, elevated serum sodium; usually
of tongue and lips, loss of skin tone haemoconcentration; high urine specific
typical gravity, low urine sodium and chloride,
normal urine sediment
anorexia, nausea, vomiting common; characteristic chest X-ray; urine shows

often dyspnoea, orthopnoea, haemop- high specific gravity, high urea, low
tysis; sometimes pulmonary rales and sodium, often proteinuria and micro-
oedema; often gallop rhythms, cardio- scopic haematuria
megaly, tachycardia; distended neck
veins; hepatomegaly, peripheral oedema
preceding pharyngitis frequent; throat cultures may be positive for

malaise, nausea, headache, anorexia streptococcus; usually elevated ASLO
common; often facial oedema; 'smokey' titre, diminished globulin; proteinuria
brown urine typical; usually mild . common; urine sediment; many RBCs
hypertension; signs of CHF in some; and WBCs; small number of renal
often pain in loins or abdomen tubular cells; granular, RBC and
hyaline casts
oedema, weight gain, hypertension often haemoconcentration, hyper-

typical in pre-eclampsia; convulsion, uricaemia; typically proteinuria;
coma in eclampsia; visual disturbances urine sediment: a few RBCs, granular
may occur; sometimes nausea, or hyaline casts
vomiting; cardiac failure may develop
weakness, anorexia, weight loss, back often rouleaux formation, elevated ESR;
pain common; sometimes peripheral usually hypercalcaemia, hyperuricaemia,
neuropathies; often bony lesions; hyper proteinuria; Bence Jones proteinuria
macroglossia may be present; normal urine sediment;
osteolytic bone lesions on X-ray;
myeloma cells in bone marrow
dry mouth, anorexia, vomiting, usually normochromic, normocytic

diarrhoea; sometimes pruritus, yellow anaemia; hyponatraemia, hyper-
complexion; heart failure in some; kalaemia, acidosis, hypocalcaemia,
often hypertension, pericarditis, hyperphosphataemia, hypermagnesaemia,
pericardial friction rub; sometimes hyperuricaemia may be present; urine
insomnia, convulsions; epistaxis, sediment: proteinuria, casts; bony
gastrointestinal haemorrhage may changes on X-ray
occur
Cardiovascular system: hypertension, pulmonary oedema,

arrhythmias from high potassium, terminal pericarditis.
Respiratory: deep sighing, breathing of acidosis (blowing off
CO 2).
Alimentary: anorexia, nausea, vomiting, hiccups, dry tongue
and stomatitis, later diarrhoea which may become bloody.
Haemopoietic: anaemia and bleeding tendency.
Nervous system: convulsions, coma, peripheral neuropathy.
Skin: brown, yellow pigmentation, pruritus, purpura.
Skeletal: bones may be decalcified (osteomalacia) calcium
deposited in tissues, or tetany may occur from a low blood
calcium.
Patients may tolerate mild symptoms for many years.

Deterioration may be provoked by infection or inadequate
fluid intake.
Investigations
The urine is oflarge volume, fixed specific gravity around 1010
and poor urea content (less than 1 gil). Proteinuria may be
present. A midstream specimen should be cultured. Frequent
weighing of the patient is a guide to fluid balance.
Straight X-ray shows small kidneys. IVP may be performed,
but the kidneys may be unable to concentrate the medium
adequately for visualization.
The blood urea [normal 2.5-7.5 mmolll (15-45 mg/dl)] is
raised: a level of 2D-30mmolll (120-180mg/dl) may be
tolerated for years, and a sudden rise is more significant than
the absolute level. The blood creatinine (another protein
metabolite) is raised and its level is independent of protein in
the diet. The creatinine clearance test is a guide to the
glomerular filtration rate, roughly parallels residual renal
function, and may drop to 10070 of normal or even less in the
terminal stage. The serum sodium, potassium and degree of
acidosis (low pH or bicarbonate) are measured.
Chapter 8
The Central and Peripheral
Nervous System
Apart from cerebrovascular disease or 'strokes', there are few

diseases of the central nervous system (CNS) that are common.
Strokes are a major cause of death - at least 10070 of all deaths
(the third commonest cause in Western countries) - but other
CNS and neurological disorders cause relatively few deaths -
less than 1070. Migraine, epilepsy, head injury, tumour,
paralysis agitans, vertigo and multiple sclerosis are the main
disorders of this system leading to either initial consultation or
hospital admission - and they occur, in incidence, in that order
of frequency in the population.

(A) central and peripheral nervous system reflexes,
(B) retina by ophthalmoscopy,
(C) X-rays - straight, scan and contrast,
(D) lumbar puncture,
(E) electroencephalography,
(F) electromyography.
137
Common symptoms of disorder will be:

(1) loss of muscular function,
(2) loss of consciousness,
(3) headache,
(4) neuralgia,
(5) dizziness and disorientation,
(6) nausea and vomiting.
(A) THE NERVOUS SYSTEM REFLEXES

The spinal reflex arc consists of the sensory fibres which
receive information from the periphery and pass it via the
posterior root into the spinal cord, where a connector neurone
passes it to the anterior horn cells, from which the stimulus
passes out to cause muscular contraction.
Damage to the reflex arc at any part of its course results in
loss of a 'deep' (or tendon) reflex such as the knee jerk,
normally produced by contraction of the quadriceps muscle
following the sensory stimulus of a tap on the patella tendon
with the tendon hammer.
The activity of the reflex arc and its lower motor neurone
fibres is influenced by the upper motor neurone.
A lower motor neurone lesion is characterized by muscle
weakness or flaccid paralysis followed by wasting, and loss of
the tendon reflexes. Groups of muscles in a limb rather than
the whole limb are involved.
An upper motor neurone lesion is characterized by muscular
weakness, that is paralysis, tending to affect the whole of one
or more limbs. There is an increase in muscle tone causing
rigidity or spasticity, and exaggerated tendon reflexes, e.g.
excessively brisk knee and ankle jerks; these may keep jerking
after the stimulus is withdrawn, the phenomenon called
clonus. There may also be abnormality of 'superficial' reflexes
with an 'extensor plantar response' (Babinski's sign) where the
big toe goes upwards and the other toes fan outwards and
upwards when the lateral border of the sole of the foot is
stroked, instead of the normal downward 'flexor' movement.
An upper motor neurone lesion is also associated with absent
abdominal reflexes - that is stroking the skin of the abdomen
THE CENTRAL AND PERIPHERAL NERVOUS SYSTEM 139
fails to elicit the normal contraction of the muscles of the

abdominal wall.
An upper motor neurone lesion causes a hemiplegia - a
paralysis of one side of the body including the lower half of the
face, the arm, and the leg. (Classically caused by a stroke -
haemorrhage or ischaemia - affecting the internal capsule
containing the pyramidal tract.) Paralysis of both legs is called
paraplegia.
A more extensive lesion in the brain may involve fibres
radiating from the optic nerves and tracts, causing loss of the
field of vision. Any lesion of the pyramidal tract may also
involve speech fibres, causing expressive dysphasia - difficulty
in finding the word. Larger lesions affecting the hearing area
or its fibres cause receptive language difficulties, and the
patient is incoherent and confused.
Small areas of destruction of the cerebral cortex may cause
apraxia, a disorder of the motor act - thus the patient may
have normal power and be able to hold a box of matches, but
he is incapable of striking a light; similarly, agnosia is a
disorder of sensory appreciation - crude sensation such as pain
and touch is retained, but the patient is unable to state the
nature of an object placed in his hand.
Apart from the sensations such as pain, temperature and
touch reaching consciousness, the sensory fibres convey
information on muscle tone and balance, proprioception, and
disturbance results in ataxia and inco-ordination of muscular
movement. Ataxia may result from destruction of the
posterior columns of the spinal cord, resulting in a reeling or
drunken gait. Inco-ordination of movement also occurs in
lesions of the cerebellum or its connections in the brain stem as
in multiple sclerosis, so that the patient 'overshoots the mark'
when trying to grasp an object and has a tremor, called
intention tremor, as he is about to reach it. Nystagmus can be
regarded as an intention tremor of the eyes when fixing on an
object, due to inco-ordination of the external ocular muscles.
(B) EXAMINATION OF THE RETINA (OPTIC FUNDUS)

WITH THE OPHTHALMOSCOPE
Papilloedema may be seen in raised intracranial pressure and
hypertension. In hypertension, arteriosclerosis and diabetes,

retinal vessel changes and haemorrhages may be visible. In
subarachnoid haemorrhage there may be a small pool of blood
at the retina.
(C) X-RAYS, STRAIGHT, SCAN AND CONTRAST

(iJ STRAIGHT X-RA YS
The skull may be invaded, or show evidence of raised intra-
cranial pressure, in cerebral tumour, but such changes are late.
A calcified pineal gland may show a shift from its normal
central position due to a space-occupying lesion. Chest X-ray
should always be carried out, for a brain tumour may be a
secondary from bronchogenic carcinoma.
(ii) COMPUTERIZED AXIAL TOMOGRAPHY

Also known as CAT scan. This form of X-ray has revolution-
ized diagnosis in neurology; it gives an anatomical picture of
the brain, and soft tissues and abnormalities such as tumours
and haemorrhage can be recognized. It is a 'non-invasive'
investigation causing no discomfort to the patient.
(iii) RADIOISOTOPE BRAIN SCANNING

Certain radioactive isotopes are selectively taken up by brain
tumours which can be detected by a counter scan or 'scanner'
over the skull.
(iv) CEREBRAL ANGIOGRAPHY (ARTERIOGRAPHY)

This is the injection of a dye, opaque to X-rays, into a blood
vessel, usually a large artery such as the carotid. Its branches
inside the skull can be seen on X-ray using a cinematograph
technique. Aneurysms and vascular abnormalities may be
identified.
(v) MYELOGRAPHY
Here an iodine-containing substance, opaque to X-rays, is

injected at lumbar puncture to show the presence of a spinal
cord blockage.
(D) ELECTROENCEPHALOGRAPHY (EEG)

A series of recordings of the electrical activity of the brain
using electrodes attached to the head. The test indicates
localized abnormality of brain function over areas of softening
or tumour and may show local or general abnormalities of
electrical activity characteristic of the several types of epilepsy.
(E) LUMBAR PUNCTURE

A specimen of cerebrospinal fluid (CSF) is obtained by insert-
ing a needle, under local anaesthesia, into the subarachnoid
space below the level where the spinal cord ends (which is
opposite the lower border of the first lumbar vertebrae). The
needle is usually inserted between the 3rd-4th or 4th-5th
lumbar vertebrae with the patient held curled-up in the left
lateral position. Lumbar puncture should not generally be
carried out if there is papilloedema, for raised intracranial
pressure may cause downward 'coning' of the brain against the
skull if fluid is taken off from below.
At lumbar puncture, the CSF pressure is measured with a
manometer, normal is 50-150 mm of fluid, and there should
be a free rise and fall on pressing and releasing each jugular
vein in turn, excluding any blockage. Normal CSF is crystal
clear, contains virtually no cells and has a protein content of
less than 0.4 gil (40 mg/dl). White cells may be increased in
inflammatory conditions and bacteriological culture will
confirm infections. The CSF is heavily blood-stained in
subarachnoid haemorrhage and sometimes after intracerebral
haemorrhage. Abnormalities in the CSF protein are
fractionated chemically; they occur in neurosyphilis, multiple
sclerosis and acute ascending polyneuritis.
(F) NERVE CONDUCTION STUDIES AND

ELECTROMYOGRAPHY
These electrical techniques may define peripheral nerve
changes and allow differentiation of nerve and muscle disease.
Common Disorders of the Central and

Peripheral Nervous System
(1) CEREBROVASCULAR DISEASE
In elderly people the cerebral arteries are very liable to be

affected by arteriosclerosis usually as part of more widespread
arterial involvement. Arteriosclerosis is a degenerative change
of the lining membrane of the artery associated with patchy
fatty deposits with tendency to thrombosis and aggregation of
platelets on the roughened surface.
The arteriosclerotic change has two effects - it narrows the
arterial lumen (which may become completely obstructed),
and the plaque is a source of emboli which may impact in a
distal, smaller artery, causing ischaemia or infarction at a
distance from the main vessel.
STROKE, CEREBROVASCULAR ACCIDENT, APOPLEXY

A stroke - a cerebrovascular accident - is an abrupt loss of
function of some part of the brain due to an arterial lesion.
The common stroke of the elderly results in hemiplegia, a
branch of the middle cerebral artery serving the internal
capsule may have been affected by thrombosis, or haemorr-
hage, or an embolism may have travelled from the heart.
Haemorrhage is more catastrophic with destruction of brain
tissue and often death. The differentiation of thrombosis and
haemorrhage may be impossible.
Many strokes are also due to arterial disease affecting the
internal carotid artery in the neck, narrowing its lumen and
being a source of emboli.
Many major strokes are preceded by transient ischaemic
attacks with impairment of function lasting less than an hour.
These little strokes are often due to small emboli from an
internal carotid artery thrombosis.
(a) Minor strokes

Symptoms and signs
Transient weakness of the arm and leg.
Blindness affecting the eye on the same side as the lesion.
A murmur ('bruit') may be heard with the stethoscope over the
narrowed internal arotid artery.
Dizziness.
Cranial nerve palsies and sometimes momentary loss of
consciousness with a 'drop attack'.
Recurrent episodes contribute to intellectual deterioration.
(b) Major strokes

Symptoms and signs
Weakness, or paralysis of one side of the body - hemiplegia.
Onset is generally sudden.
Frontal headache.
Dysphasia may occur from involvement of the speech centre.
Disturbance of cerebration, or the patient may be found
unconscious.
Deepening coma with no response to commands or to painful
stimuli.
Stertorous or periodic breathing of Cheyne-Stokes type.
Pulse slow but full.
Incontinence of urine.
In severe cases, all four limbs may be flaccid, both plantar
responses extensor and deterioration may be rapid with death
in hours or a day or two.
In the majority of strokes, however, the lesion is an ischaemic

rather than a haemorrhagic one, and consciousness is quickly
regained or improves over hours or a few days. The paralysis
affects the lower half of the face, the arm and the leg, but the
limbs may be initially flaccid and remain so, or develop the
classical spasticity of the upper motor neurone lesion, with
extensor plantar response. Difficulty in swallowing and artic-
ulation is usually transient.
A hemiplegia may be accompanied by loss of sensation on
the paralysed side, and if the lesion is more extensive, involve-
ment of the optic radiation causes loss of one half of the visual
field - thus a lesion in the left internal capsule can cause right
hemiplegia, dysphasia, right hemi-anaesthesia, and right
hemianopia - the patient may not be aware of objects on the
right side of his body and may ignore that side.
There is usually little difficulty in distinguishing a stroke
from other neurological conditions - a stroke is a vascular
occlusion or haemorrhage and of sudden onset, distinct from
the gradual onset of symptoms from a cerebral tumour.
Regular observations - of level of consciousness, pulse,
blood pressure, respiration, temperature, fluid intake and
urine output - should be made. Deterioration of conscious-
ness, a slowing pulse and rising blood pressure suggest rising
intracranial pressure or cerebral destruction. Hyperpyrexia,
with pinpoint pupils, may occur in haemorrhage.
(2) INTRACRANIAL HAEMORRHAGE

The forms of brain haemorrhage are:
(i) Intracerebral haemorrhage
As in 'Stroke' above.
(ij) Subarachnoid haemorrhage

Due to rupture of a small aneurysm of one of the arteries at the
base of the brain. The aneurysm forms as a result of a develop-
mental defect in the vessel wall, and it manifests in adult life.
Symptoms and signs

Commonest in young and middle-aged adults.
Warning headache or neckache.
Days later the patient suffers severe and often agonizing

headache and neckache with neck stiffness.
Sudden loss of consciousness with deep coma and flaccid
weakness of all limbs.
Diagnosis is confirmed by lumbar puncture which reveals
heavily blood-stained cerebrospinal fluid.
CAT scan shows the site of haemorrhage and may reveal the
aneurysm causing it.
Angiography subsequently allows detailed assessment of the
aneurysm and blood vessels.
(iii) Extradural haemorrhage
This follows a head injury, usually with fracture of the

temporal bone of the skull, and is due to rupture of the middle
meningeal artery.
The patient may have been transiently stunned, then there is a
'lucid interval', and then deepening coma from the pressure
effects of the bleeding displacing the brain - there may be a
dilated pupil.
CA T scanning and surgical aspiration of the haemorrhage are
indicated.
(iv) Subdural haemorrhage

A more slowly developing collection of blood from ruptured
veins in the subdural space.
It occurs in birth injury, and also in the elderly, possibly
because of some shrinkage of brain substance and weakening
of the walls of the veins, which rupture after relatively trivial
injury.
A history of injury to the head, which may have been
forgotten, and the skull mayor may not have been fractured.
Days or weeks later there is disturbance of consciousness or
lateralizing signs, and the condition may be mistaken for a
stroke. The subdural haemorrhage is one form of 'space-

occupying-lesion' and the treatment is surgical.
(3) SPACE-OCCUPYING LESIONS OF THE BRAIN

These are haematomas, cerebral tumours or abscesses.
Symptoms and signs

(i) L Deal effects
By destroying the brain substance, the lesion may cause
complaints such as difficulty in moving part of a limb, or
disorder of the motor act (apraxia).
Speech disturbance, transient deafness or defective sense of
smell.
The personality may change with behaviour disorders, e.g.
inappropriate urination.
There may be focal fits related to disturbance in electrical
function.
(ii) Displacement effects

A nerve may be displaced and stretched - thus there may be
paralysis of the sixth cranial nerve with resultant orbital muscle
weakness and double vision (diplopia)
A tumour such as the 'acoustic neuroma' not only causes
deafness and ataxia (disturbance of gait) but also causes loss of
the corneal reflex from stretching of the fifth and seventh
cranial nerves.
(iii) Raised intracranial pressure

Diffuse pressure effects on brain metabolism and disturbance
of the normal circulation of the cerebrospinal fluid.
Headache.
Vomiting.
Drowsiness.
Slowing of the pulse and of the respiratory rate.
Papilloedema.
Confirming the presence of space-occupying lesion
Skull X-ray may show a displacement of the pineal gland from
the midline should the gland be calcified as it often is in middle
age; some tumours are calcified.
Raised intracranial pressure may cause erosion of the bone
near the pituitary fossa - which can itself be enlarged in
pituitary tumour.
Chest X-ray may show a primary tumour in the lung.
CAT scanning shows the site and often the nature of the lesion.
Isotope scanning and EEG may be useful in confirmation.
(4) INFECTIONS OF THE CENTRAL NERVOUS SYSTEM

(iJ MENINGITIS
An acute inflammation of the meninges, usually bacterial,
spread having occurred from a septic process penetrating the
skull following injury or operation, or via the bloodstream
from a distant focus, e.g., the throat.
Symptoms and signs

Meningococcal meningitis is commonest in young people,
especially in closed communities which may allow spread of
infection from throat or nasal secretions.
Onset is usually acute with headache, neck ache and neck
stiffness.
Inability to straighten the knee when the hip is flexed (Kernig's
sign) - due to the inflamed meninges irritating the nerve roots.
Clouding of consciousness.
Diagnosis is confirmed by lumbar puncture. The cerebrospinal
fluid may be under raised pressure, is cloudy due to pus cells in
the bacterial cases and the organisms can be cultured from it.
(iiJ ENCEPHALITIS AND ENCEPHALOMYELITIS

The enteroviruses, which include the poliomyelitis, Echo and
Coxsackie viruses, spread in the bloodstream to reach the
nervous system and cause an encephalitis, an inflammation of

the brain cells, or in the case of poliomyelitis the virus tends to
localize at the anterior horn cells of the spinal cord.
The virus of herpes simplex, which normally cause only
'cold sores' at the mouth, can at times cause a severe encephal-
itis; similar viruses are responsible for epidemics of encephal-
itis occurring in the tropics and the Far East.
The childhood fevers - measles, mumps, rubella (German
measles) and chickenpox - may be accompanied or followed
by virus invasion of the nervous system resulting in encephal-
itis or encephalomyelitis and mild meningitis. Encephalo-
myelitis may also follow glandular fever (infectious mononu-
cleosis), and vaccination against measles and smallpox.
Encephalomyelitis is characterized by patchy demyelination
of the insulating and nutritive myelin sheath that surrounds the
nerve fibres in the brain and spinal cord. Demyelination may
also involve the peripheral nerves.
Symptoms and signs

Often mild, and the illness transient.
In severe cases there is fever, disturbance of cerebration with
intellectual disturbance, emotional upset and clouding of
consciousness. The patient resents interference.
Sleep rhythm may be upset.
Headache.
Vomiting.
Neck stiffness.
Cranial nerve palsies and additional motor or sensory impair-
ment from peripheral nerve involvement.
At lumbar puncture, the CSF may be normal or show
increased cells or protein.
Blood may show a rising virus antibody titre.
Virus may be cultured from the stools, in which enteroviruses
survive for up to 24 h at room temperature.
The EEG may show diffuse electrical disturbance of the brain.
(iii) RABIES
Rabies is a virus infection which results in a form of encephal-
itis, usually fatal. The virus is transmitted to humans through
bites from infected animals, especially dogs, but bats are also
carriers. If a person is bitten, he must be given an immediate
course of anti-rabies vaccination, otherwise the virus passes up
the nerves to reach the brain.
Symptoms include
Muscular stiffness.
Convulsions.
Paralysis of swallowing.
Coma and death.
(iv) POLIOMYELITIS
This is increasingly rare due to effective vaccination. The
poliomyelitis virus is of the enterovirus group, colonizing in
the intestinal tract and excreted in the faeces. Thus infection is
still common in underdeveloped countries with poor hygiene
and primitive sanitation. The virus spreads to the CNS,
affecting mainly the anterior horn cells of the spinal cord,
though the brain stem may also be involved.
Symptoms and signs

Initial febrile illness, often with signs of meningeal irritation.
Followed by paralysis of sudden onset, usually affecting one
leg or arm.
If the phrenic nerve supplying the diaphragm, and the nerves
to the intercostal muscles, are involved, respiration becomes
impossible.
Involvement of cranial nerves results in difficulty in speaking
and swallowing, and the respiratory centre in the medulla can
also be affected.
(v) HERPES ZOSTER (SHINGLES)

This is a virus infection of the posterior (sensory) nerve root
ganglia. The virus is the same as that causing chickenpox in

children. Herpes zoster is commonest in the middle-aged and
elderly, the virus possibly lying dormant in the nervous system.
The condition may only appear if the patient is debilitated, or
it may accompany an irritative lesion such as a tumour near the
nerve root.
Symptoms and signs

'Herpes' describes the herpetic or vesicular eruption, and
'zoster' means its band-like distribution along the line of a
nerve, often an intercostal nerve.
A painful, itchy vesicular rash commonly at the trunk, but any
nerve can be involved.
The ophthalmic division of the fifth (trigeminal) cranial nerve
may be affected with typical rash on one half of the forehead,
and painful redness of the eye.
(vi) TETANUS (LOCKJAW)
The spores of the bacillus Clostridium tetani causing tetanus

are found in manure, soil and dust. Like the gas gangrene
organisms, the tetanus bacilli grow best where the oxygen
supply is poor, and infection follows contamination of deep
punctures and wounds.
Tetanus is due to a toxin produced by the bacilli growing in a
wound. This toxin travels up the peripheral nerves to reach the
eNS.
(vii) BOTULISM
Botulism is a form of food poisoning due to a bacterial toxin
which blocks the release of acetylcholine at nerve endings,
causing widespread paralysis. The spores of the bacillus
producing the toxin (Clostridium botulinum), like those of
tetanus, are found in soil and faeces. They multiply in
anaerobic conditions as in canned foods or home-bottled fruit
which has been inadequately sterilized. The spores themselves
resist boiling but the toxin is easily destroyed by cooking.
Symptoms and signs
Some vomiting but seldom pain or diarrhoea.
The absorbed toxin paralyses nerve endings.
Difficulty in talking and swallowing.
Double vision and giddiness.
Paralysis extends to the trunk and limbs and death may follow
from respiratory failure.
(5) MULTIPLE SCLEROSIS (DISSEMINATED

SCLEROSIS)
Multiple sclerosis is a chronic disease of the nervous system,
almost always arising before the age of 40. It is characterized
by remissions and relapses and by the presence of multiple
patches of sclerosis scattered throughout the brain and the
spinal cord.
Cause
The cause is unknown. The disease affects 1 in 2000 of the
population of the UK and the USA, is commonest in temperate
northern climates, rare in the tropics and South Africa, and
unknown in China and Japan. Multiple sclerosis is a demyelin-
ating disease - the myelin sheath, which protects and nourishes
the nerve fibre Gust as insulation protects an electric cable) is
destroyed by some unknown agent. Conduction in the under-
lying nerve fibres is at first only temporarily affected, and early
changes may be reversible, but later, plaques of scar tissue are
formed, destroying the nerve fibres.
The demyelination bears some resemblance to lesions in
encephalomyelitis and a virus cause has been suggested, or an
infective agent, aggravated by stress, injury, infection or in the
puerperium. Multiple sclerosis may be a disturbance of
immunity resulting in change in the fatty acids of the myelin
sheaths.
Symptoms and signs

These are disseminated - in time and in place.
The presenting sign is often a transient weakness of arm or leg

or a blurring of vision which clears up.
Months or years later there are more permanent signs.
The pyramidal tracts are commonly involved causing spastic
weakness, becoming fairly symmetrical in both legs.
Sensory changes are slight.
There is often disturbance of bladder function such as urgency
of micturition, incontinence, or retention.
Cranial nerve involvement includes the optic nerve causing the
visual disturbance and sometimes pallor of the optic disc seen
with the ophthalmoscope.
The cerebellum and its connections may be involved, causing
disorder of muscle balance and control and ataxia.
There is a fine tremor of the fingers, more marked on
movement (intention tremor) and brought out by the
'finger-nose' test, as the patient, starting with hand
outstretched, brings in the index finger to touch the tip of the
nose.
There is inability to perform rapid to-and-fro movements of
the hands.
A similar disturbance of the ocular muscles causes the fine
tremor of the eyes, called nystagmus, when attempt is made to
fix the gaze on an object held in front.
The voice may have a peculiar staccato quality.
There may be acute exacerbations of symptoms, settling in
early cases and followed by months or even years of remission.
In severe cases there is gradual deterioration over the years, the
patient becoming paraplegic (paralysed in both legs) and
incontinent, unable to get out of bed without help, and prone
to urinary and chest infections and to pressure sores.
Lumbar puncture. In half the cases of multiple sclerosis, the
cerebrospinal fluid shows an increase in the gammaglobulin
fraction of the protein.
Apart from routine ones such as urine testing, blood count and
chest X-ray, further investigations are seldom required, but
myelography may be indicated in the occasional patient with
purely pyramidal tract signs, to exclude a tumour or other
lesion causing compression of the spinal cord.
(6) SYNCOPE
This is transient loss of consciousness due to inadequate

cerebral blood flow.
(i) FAINT (VASOVAGAL A TrACK)

Occurs in healthy people, usually the young, and is a feeling of
light-headedness which is followed by collapse - the person
has some warning of an impending faint.
Causes
Precipitating factors may be psychogenic - emotion, an
unpleasant sight, fear of an injection, or the presence of severe
pain (cardiac pain, renal 'colic'). These result in vagal stimul-
ation with lowered peripheral resistance and pooling of blood,
causing reduced venous return and cardiac output. The heart is
also slowed. Prolonged standing in the erect posture in a hot
climate also causes venous pooling, with the same result.
Symptoms and signs

Pallor.
Sweating.
Feeling of sickness and swimming in the head.
Loss of consciousness and collapse.
The pulse is slow and the blood pressure lowered, but as soon
as the person is flat, the cerebral circulation improves and
consciousness returns in a few seconds.
(ii) CARDIAC SYNCOPE
This occurs in the older age groups, and usually there is a

known history of heart disease. Fainting occurs on effort in
patients whose hearts cannot meet the demand for blood
created by exercise, and there is temporary cerebral anoxia -
this may occur in aortic stenosis or mitral stenosis.
Stokes-Adams attacks are sudden episodes of cerebral anoxia
following heart block, with return of consciousness and facial
flushing when the ventricle restarts. The onset of atrial fibril-
lation or other arrhythmia may also cause temporary cerebral
ischaemia.
Sino-atrial disease ('sick-sinus syndrome') associated with
rhythm disturbance and sinus arrest, may have similar effects
in the elderly.
Carotid-sinus syncope is due to pressure of a tight collar
stimulating the carotid sinus nerves with resultant reflex hypo-
tension.
Cough syncope ('cough drop') occurs when a patient,
frequently a chronic bronchitic, coughs so much that he
impedes the venous return to the heart, resulting in collapse.
(7) EPILEPSY
A group of conditions characterized by r~current attacks of
disordered brain function called seizures or fits. Fits are of
sudden onset and each is usually short in duration, lasting only
a matter of minutes.
Cause
Epilepsy results from disordered electrical activity of the
brain. The fit is due to an abnormal electrical focus firing off a
discharge with resultant disturbance of cerebration and
usually loss of consciousness.
TYPES OF EPILEPSY
Symptomatic epilepsy
Due to some definable irritant focus, the epilepsy is a symptom
of the underlying disorder. Thus epilepsy may follow damage
to the brain at birth, or head injury, or indicate the presence of
a space-occupying lesion such as tumour, abscess or
haematoma, or result from a scar of the brain after a stroke.
Idiopathic epilepsy
In the vast majority of cases of epilepsy, no reason for the
electrical instability can be discovered - 80070 of the patients
belong to this group.
The incidence of known epilepsy is 5 per 1000 of the
population but the condition may go unrecognized, and many
people have an epileptic attack at some time during their lives.
There is a familial tendency, the incidence of epilepsy in the
children being slightly higher if one parent is affected, and
considerably higher if both parents have known epilepsy.
Factors precipitating an attack include fatigue and stress,
over-hydration, anoxia and metabolic causes such as uraemia,
hypo glycaemia and hypocalcaemia. Fits also occur in severe
toxaemia of pregnancy - eclampsia. A flickering television
screen may provoke a fit due to the stroboscopic effect. More
often, no precipitating cause can be recognized.
PETIT MAL - MINOR EPILEPSY

Symptoms and signs
Arises in children or adolescents and never starts in adult life.
A transitory interruption of consciousness, without any
convulsive element. The patient simply stops what he is doing
or saying and may stare vacantly into space for a few seconds
before resuming his previous activity. He seldom, if ever, falls,
and he has no realization that anything abnormal has
occurred.
Attacks may occur once every few weeks or months, or there

may be several in one day.
Diagnosis should be possible from a description of the attacks,
and can be confirmed by the electroencephalogram, which
shows a characteristic spike-and-wave pattern.
GRAND MAL - MAJOR EPILEPSY

This commonly begins between the ages of 7 and 17. Attacks
starting in adult life should raise the suspicion of a brain lesion
such as a tumour. The fit is almost always of sudden onset and
has three stages:
The major fit

Tonic stage
The patient may cry out, consciousness is suddenly lost and he
falls to the ground.
All the muscles are in rigid spasm, so he falls heavily and may
injure himself.
The limbs are extended, the jaw clenched and the tongue may
be bitten.
Respiration ceases, resulting in cyanosis. (This tonic stage lasts
for about half a minute.)
Clonic stage
Muscle twitching often starts at the fingers or around the
mouth, then the limb muscles contract and relax, causing
jerking movements.
These movements spread, becoming violent and convulsive,
the arms and legs thrashing about with risk of further injury,
but breathing is resumed.
The muscle jerkings involve the jaw and mouth, so the tongue
may be bitten again and with foaming of the saliva the patient
froths at the mouth.
There may be incontinence of urine. (This stage lasts for
1-3 min after which the movements gradually cease.)
Somnolent stage
The patient now passes into a deep sleep or coma, remaining
unrousable for a few minutes or up to an hour.
During this, and the clonic stage, the pupils and reflexes may
be abnormal with extensor plantar responses.
The patient may subsequently feel drowsy and sometimes

complains of headache.
Amnesia.
Occasionally there is a period of post-epileptic automatism
during which the patient may carry out some action of which
he is unaware.
Status epilepticus
The occurrence of a series of major fits, the patient passing
from one fit to another without regaining consciousness. The
patient may become hyperpyrexial, and the periods of anoxia
may precipitate brain damage.
Further investigations in grand mal

It is essential to obtain an eye-witness account of the fit and
usually this allows diagnosis.
Electroencephalography
The EEG shows an electrical abnormality of the brain which
may be of localizing value, or it may be generalized.
Most cases of epilepsy are idiopathic, but the fact that the
condition may be a symptom of an underlying lesion such as a
tumour should be borne in mind, especially where fits start in
adult life.
A full clinical examination, including ophthalmoscopy and
urine testing, blood count and blood sugar estimations, and
X-rays of chest and skull are necessary but if a space-occupying
lesion is suspected CAT scan is indicated. Lumbar puncture
need not be done routinely but a raised CSF protein would
heighten a suspicion of tumour.
(8) HEADACHE
Headache is a common symptom which generally has no
serious cause, but it can be associated with organic disorder.
The brain itself is insensitive to pain but intracranial structures
such as the arteries and meninges are pain-sensitive. Spasm of
the cervical muscles also results in pain.
Causes of headache
(i) Vascular
The headache accompanying fever is probably due to

dilatation of intracranial arteries. Migraine headache (see
below) is due to dilatation of extracranial arteries in the
external carotid system. The same mechanism explains the
headache that may occur with internal carotid artery
thrombosis.
Headache may occur in cerebral haemorrhage before
consciousness is lost - in subarachnoid haemorrhage there is
severe occipital headache and neck stiffness, and there may
have been a prolonged neck -ache from leakage of the aneurysm
aneurysm a few days earlier.
Temporal (cranial) arteritis is one of the connective tissue

autoimmune diseases, and is an inflammation of the arteries of
the skull, with headache and tenderness at the temple, usually
unilaterally. The condition may involve the retinal arteries,
leading to blindness, and it is commonest in elderly men. The
ESR is raised.
(ii) Tumour and raised intracranial pressure

Tumour may cause headache which is dull in character, rarely
severe and tends to occur early in the day.
Though raised intracranial pressure from any cause, can
produce a generalized headache, its intensity need not be
related to the height of the pressure.
(iii) Inflammation and irritation
Meningitis and encephalitis can cause severe headache. There

is also neck-ache and neck stiffness. Occipital headache and
neck stiffness occurs also in subarachnoid haemorrhage.
Sinusitis - stuffy, headachy feelings and tenderness over the
affected part.
Eye causes - 'eye strain' from refractive errors may cause
evening headaches. Glaucoma - raised intraocular pressure,
with risk of loss of vision, and often accompanying vomiting-

is a cause of headache in the elderly.
(iv) Cervical spondylosis - 'tension' headache

This is a form of arthritis affecting the cervical spine. There is
associated muscle spasm with pain and tenderness at the neck,
often spreading to cause a generalized headache. Symptoms
are worse in tense, anxious patients, their state probably
contributing to increased muscle tension - 'tension' headache.
(v) Depression
Depression and psychogenic factors lie behind many chronic
or recurrent headaches, muscle tension making the symptoms
worse.
(vi) Migraine
Migraine is recurrent attacks of headache, often in bouts for a

week or two, then there may be freedom for months. Migraine
begins in adolescence, often there is a family history and
attacks tend to be less severe after middle age. Sufferers are
often of a tense, worrying personality. Attacks may occur pre-
menstrually. possibly due to fluid retention.
Symptoms and signs

The 'aura' - due to spasm of intracranial arteries - may
present as 'flashing lights' or visual upset, minutes or even
some hours before the next stage.
Headache is often localized to the region of the superficial
temporal artery on one part of the head, and it is usually the
same part that is involved in each attack.
The headache may be so severe that the patient has to lie down
in a dark room to gain relief.
Occasionally there is weakness of a limb or one side of the body
(hemiplegic migraine).
Nausea and vomiting - may complicate or follow the
headache.
(9) PARALYSIS AGITANS

A chronic and progressive disease due to degenerative changes
in the basal ganglia of the brain; it is a common condition in
the middle-aged and elderly.
Cause
In all types there are degenerative changes in the basal ganglia,
the nuclei at the base of the brain or their connections, which
form part of the extrapyramidal system concerned in normal
muscle tone. It is associated with depletion of a substance
called dopamine, a neurological chemical transmitter.
Dopamine regulates the function of the extrapyramidal
system, and lack of it results in the increased muscle tone of
paralysis agitans or Parkinsonism.
Types
(i) Idiopathic
The cause of the degenerative change in the basal ganglia is
unknown. This is the common form of this disease, developing
insidiously between the ages of 50 and 65, being commoner in
men, and there is a slight familial tendency.
(ii) Arteriosclerotic
The degenerative changes are vascular in origin. The condition
occurs in the elderly and is accompanied by other evidence of
cerebral arteriosclerosis. There may be a history of strokes,
and sometimes a degree of dementia.
(iii) Drug-induced
Phenothiazine drugs such as chlorpromazine, and
methyldopa, reserpine and metoclopramide, may interfere
with the action of dopamine or other neurochemical
transmitters. There may be crises of abnormal jerky
movements (dystonia) with rigidity and fixed upward gaze of
the eyes.
Symptoms and signs

Tremor is often the presenting sign, and is described as a 'pill-
rolling' movement or shake of the fingers.
Tremor becomes more marked if the patient is engaged by the

examiner in conversation, or is emotionally upset.
It may disappear on performing a voluntary movement and is
absent during sleep.
Rigidity of the muscles; the patient has difficulty holding a pen
and the writing becomes smaller.
The muscular rigidity causes a 'poverty of movement' with
lack of blinking and a loss of the normal facial expression,
producing a 'mask-like' face.
A walk with short, shuffling steps.
Voice becomes low and monotonous and all movements are
performed slowly.
Though the muscles have increased tone, there are no reflex
changes and no true paralysis, rather a restriction of
movement.
Bladder function is preserved.
When the forehead of the patient is tapped, he keeps on
blinking.
(10) SPINAL CORD COMPRESSION

The spinal cord runs from the foramen magnum of the skull,
where it is continuous with the medulla, and ends at the lower
level of the first lumbar vertebra. In its course, it gives off and
receives the motor and sensory nerve roots, being protected in
front by the bodies of the vertebrae (separated by the discs) and
surrounded by the neural arches of the vertebrae behind.
Causes of spinal cord damage

Compression
(i)
Trauma - following crush fractures, or fracture-dislocation of
the vertebrae.
Vertebral disease and spontaneous fracture, as in tumour or
myeloma, causing their sudden collapse.
Prolapsed intervertebral disc in the cervical (or dorsal) spine.
Tumour- neurofibroma - may be inside the cord, or affect the

meninges or nerve root.
Secondary - metastases from carcinoma (lung, breasts,
prostate) or deposits in Hodgkin's disease.
Extradural abscess - often staphylococcal from sepsis else-
where.
(ii) Arteriosclerosis
Thrombosis of the anterior spinal artery which serves the
upper and anterior part of the cord.
(iii) Transverse myelitis

As part of encephalomyelitis.
Symptoms and signs

Transection of the cord above the fourth cervical level is
incompatible with life.
Transection at a lower level causes paralysis below the lesion;
quadriplegia is paralysis of arms and legs, the more common
paraplegia is paralysis of the legs.
Complete loss of sensation below the lesion.
Disturbance of micturition and sometimes defaecation.
Hypotension and loss of sweating.
X-ray of spine (which may show vertebral involvement).
Lumbar puncture: blockage of the CSF circulation may be
revealed by compressing each jugular vein in turn, when the
normal rise and fall of CSF pressure will be absent. Complete
blockage causes yellow CSF with a high protein content, so
that it may actually coagulate.
Myelography will localize the level and may indicate the nature
of the spinal block.
CA T scan may be helpful in localizing the lesion.
(11) DISORDERS OF THE NERVE ROOTS AND
PERIPHERAL NERVES
A nerve fibre can be involved by disease anywhere in its long
course from the spinal cord to the periphery. The fault may lie
in the nerve cell or its axon (peripheral process), in the insul-
ating myelin sheath, or in the connective tissue binding the
fibres to form the nerve trunk. The fault can be the result of
many processes: compression and irritation, inflammation,
infection and metabolic or vascular upset. Involvement of the
nerve fibres leads to impairment of conduction, whether
motor or sensory, and this may be followed by degeneration.
The vertebral bodies are separated by the intervertebral
discs. With advancing age the discs tend to 'dry', causing
stresses on the spinal joints and resulting in a form of degener-
ative osteoarthritis with the formation of bony outgrowths
called 'osteophytes' at the vertebral margins. These encroach
on the nerve roots. There is also a varying degree of backward
prolapse of the degenerate disc. The process is termed
'spondylosis', and it affects the parts of the spine which have
most movement.
(a) CERVICAL SPONDYLOSIS

Symptoms and signs
Irritation and compression of the nerve roots serving the
shoulder and arm, usually more marked on one side.
Aching at the neck, and neck movements are restricted.
Muscle spasm and tenderness.
Discomfort, tingling sensation, or pain is felt in the part of the
arm served by the affected nerve root or roots, the outer
(radial) border of the arm being commonly involved.
There may be some diminution of appreciation of light touch
or pin-prick within the affected dermatome (the area of the
skin supplied by that nerve), but complete sensory loss is
unusual.
There may be some diminution of the tendon reflexes in the
arm.
X-rays of the cervical spine will confirm the existence of

spondylosis.
(b) ARTHRITIS OF THE LUMBAR SPINE

Symptoms and signs
The degenerative changes in the lumbar spine may be a cause
of low backache or lumbago.
May occur acutely after sudden flexion, as in stooping to pick
up a heavy weight.
Sudden pain down the back of the thigh and leg - 'sciatica'.
There may be loss of the ankle jerk and pain on attempting to
raise the leg to a right angle.
(12) DISORDERS OF PERIPHERAL NERVES
ENTRAPMENT NEUROPATHIES
(a) Cervical
An extra, cervical, rib, or anomalies of structures between the
first rib and the clavicle cause narrowing of the cervical outlet,
resulting in pressure on the brachial plexus and nerve trunks.
Symptoms and signs

Sensory disturbance usually along the inner (ulnar) border of
the arm and hand.
Muscle weakness and wasting.
Symptoms might be worsened by drooping of the shoulder
girdle or the carrying of heavy weights.
(b) Carpal tunnel syndrome
The median nerve may be compressed as it passes through the

fibrous tunnel at the wrist on its way to serve the hand.
Symptoms and signs

Pain and tingling in the hand and fingers, especially those on
the medial side of the hand, often occurring by night.
Discomfort felt at the wrist with tenderness over the fibrous

tunnel.
Wasting of the small muscles at the base of the thumb, some of
which are supplied by the median nerve.
Common in middle-aged women and is sometimes associated
with arthritis or undue use of the wrist.
It may also occur in pregnancy, from fluid retention and tissue
swelling; and in myxoedema (hypothyroidism) and
acromegaly (a result of hyperpituitarism).
Ie) Trauma
In the arm, the radial nerve is very liable to be damaged in its

long winding course round the humerus - and it may also be
affected in the axilla from prolonged hanging of the arm over a
chair ('Saturday night' or 'drunkards' paralysis). The radial
nerve is mainly motor, and the lesion results in inability to
extend the wrist and fingers.
PERIPHERAL NEUROPATHY
In this group of conditions the peripheral nerves are symmet-
rically involved. The longer the nerve fibre, the more liable it is
to be damaged. Thus there are varying degrees of sensory
disturbance and muscular weakness in the feet and limbs.
Causes
(i) Toxic
Lead, arsenic and heavy metals. Lead poisoning (e.g.
inhalation of fumes from the burning of car batteries) causes
motor-weakness without sensory loss (also constipation,
anaemia and a 'blue' lead-line on the gums).
Triorthocresyl phosphate (TOCP) and acrylamide, both used
in the plastics industry.
(ii) Deficiency
Vitamin Bl; dry beri-beri may be due to multiple dietary defici-
encies rather than deficiency of Bl alone, and occurs in the
DIFFERENTIAL DIAGNOSIS OF LOSS OF CONSCIOUSNESS

Onset and duration Pre-existing
symptoms or conditions
Intracerebral abrupt and continuing hypertension; more common

haemorrhage in elderly; headache;
hyperthermia later
Subarachnoid warning headache; may be minor head injury;

haemorrhage abrupt loss of consciousness headache, neck stiffness;
may be days later more common in young
Extradural transient stunning; initial follows head injury; prob-

haemorrhage lucid intervals; deepening able fracture, temporal skull
coma gone; vomiting, drowsiness
Cerebral tumour slow, preceded by motor, sensory, speech or

neurological symptoms; loss visual disorder, headache,
of consciousness late in vomiting or development of
disease process convulsions
Syncope sudden, transient, spon- sweating, psychogenic anxiety,

taneous recovery most often in adolescent -
young adult
Meningitis clouding of consciousness neck stiffness, fever, vomiting;

slow as disease advances sepsis focus - e.g. throat,
respiratory tract
Epilepsy abrupt after warning 'aura', more common in young, may

(grand mal) tonic and clonic stage, be idiopathic or late
spontaneous recovery; may consequence of skull injury,
be frequent, recurrent or cerebral space-occupying
attacks lesion
hemiplegia; deepening coma, blood-stained CSF, increased

flaccidity of limbs, incon- CSF pressure
tinence of urine; Cheyne-
Stokes respiration
flaccid weakness all limbs CSF heavily blood-stained;

brain scan shows site, angio-
graphy shows aneurysms
dilated pupil one-sided, flaccid brain scan shows space-occupying

paralysis, papilloedema lesion one side; skull X-ray
shows fracture
papilloedema; primary Ca skull X-ray displacement of

may be in lung; cachexia if pineal gland, or fossa erosion;
metastases brain scan shows lesion, EEG
abnormalities
slow pulse, hypotension, all investigations normal

nausea; no neurological
abnormalities
photophobia lumbar puncture - raised CSF

pressure, pus cells, leukocytosis
muscle and limb twitching, CSF normal, EEG shows typical

violent, incontinence of 'spike' activity
urine, rigidity of limbs,
cyanosis; post-epileptic
confusion and amnesia
underdeveloped countries. Alcoholic neuropathy is probably

due to similar B vitamin deficiencies, for alcoholics tend to
neglect their food, but alcohol may have a direct toxic effect on
the nerves. In vitamin B12 deficiency peripheral neuropathy
can occur.
(iii) Metabolic
Diabetes; loss of sensation at the feet with tendency to ulcer
formation, absent vibration sense and reflexes.
Porphyria; a group of conditions due to an inherited disturb-
ance of haemoglobin metabolism or liver defect.
(iv) Infective and inflammatory

Acute infective (ascending) polyneuritis - (Landry-Guillain-
Barre syndrome) occurs after infection, especially respiratory
infection, or after glandular fever (infections mononucleosis),
and may be a disturbance of immunity.
Leprosy.
Diphtheria - due to toxin - paralysis of palate or limbs.
(v) 'Connective-tissue' (collagen-vascular) diseases

'Autoimmune diseases' - group includes rheumatoid arthritis,
but polyarteritis nodosa, an inflammation of arteries and
nerves affecting middle-aged men, is the usual cause in this
group.
(vi) Carcinoma - carcinomatous neuropathy

Carcinoma, especially bronchogenic carcinoma, may be
associated with distal sensory changes or sometimes a mixed
motor and sensory neuropathy. Cause possibly a toxin
produced by the growth.
Symptoms and signs

The sensory disturbance includes complaints such as
numbness, paraesthesiae (pins and needles) and pain.
Loss of sensation to pain (pin-prick), temperature and touch.
Often affects feet and ankles, and sometimes the hands, and is
described as 'glove and stocking' anaesthesia.
The motor weakness affects the distal muscles causing
paralysis of dorsiflexion of the feet and 'foot drop'.
The ankle and knee jerks are absent.
Chapter 9
The Skeletal System
The commonest disorder of the skeletal system will be, with

age, osteoarthritis. Musculoskeletal pains cause 10070 of all
medical consultations, of which one-third will be ,for
backache. Apart from trauma and the effects of ageing,
rheumatoid arthritis is the single most frequent disorder of this
system that will lead to periodic hospitalization.

(A) X-rays,
(B) blood tests,
(C) biopsy,
(D) arthroscopy.

(1) pain,
(2) loss of function, or restricted movement,
(3) swelling of the affected joint(s).
171
(A) X-RAYS
Straight X-rays of affected joints or bones may reveal
abnormalities in porosity, outline or structure. Bone scanning
using radioactive isotopes may be necessary to reveal
metastases.
(B) BLOOD TESTS

To ascertain white count changes, ESR, uric acid levels and
rheumatoid factors are necessary, as are assessment of the
blood count, LE latex and antinuclear antibody levels.
(C) BIOPSY
Biopsy of joint or muscle tissue may be necessary to confirm
diagnosis, and this can be done at the same time as:
(D) ARTHROSCOPY
The visualization, by means of fibre-optics, of the inside area
of affected joints, e.g. the knee.
Common Disorders of the Skeletal System

(1) RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a chronic arthritis· of small joints. It

may cause only slight disability, or result in crippling
deformities. It affects over 3OJo of the population and is three
times commoner in females. It usually presents in young adults
in their thirties and forties.
There is inflammation and proliferation of the synovial
lining membrane of many joints, which may proceed to cause
their destruction.
The fundamental cause is unknown. It is thought that some
environmental trigger factor, possibly a virus, stimulates the
production of antibodies causing an autoimmune reaction.
Immune complexes are deposited in the synovium (and blood
vessel walls) causing enzyme release and joint inflammation.
THE SKELETAL SYSTEM 173
Symptoms and signs
Aching pain.
Stiffness.
Swelling of the joints, especially the smaller joints.
Often worst in the morning, when there is pain and stiffness in
the fingers passing off in an hour or two but recurring the next
day.
Onset may be acute with severe pain and swelling of joints and
tendon sheaths, and the forming of rheumatoid nodules near
the elbows.
Constitutional upset includes fever, fatigue, loss of appetite,
loss of weight and anaemia.
Rheumatoid factor is detectable in the blood by the Rose
Waaler test or the RA (rheumatoid arthritis) latex test.
Blood count shows anaemia, raised white cell count, and high
ESR.
X-rays show joint deformity and adjacent bone rarefaction
(osteoporosis) .
(2) OSTEOARTHRITIS
Osteoarthritis is a degenerative disorder of the larger, weight-
bearing joints. It results from a wearing away of the cartilage
on the opposite bone surfaces. Trauma and obesity contribute
to it, and it is very common in the hips and knees of fat,
middle-aged and elderly people. There is no systemic upset,
but there may be an associated slight degenerative joint change
in the terminal interphalangeal joints of the fingers.
Symptoms and signs

(a) Limb joints
Pain and stiffness with creaking and grating of the large joints,
especially after a period of immobility.
Cold and damp may precipitate an attack.
In severe cases there is joint deformity and destruction, and in

the hips and knees this can result in serious disability and
crippling.
(b) Arthritis of the spine

Changes are especially liable to occur in the cervical spine in
association with disc degeneration (cervical spondylosis).
Aches at the neck and restricted movement, often with tender-
ness and spasm in the surrounding muscles.
Nerve root pressure may cause discomfort in the arms.
Lumbar region arthritis may be associated with the low
backache and disc degeneration and prolapse may cause
'sciatica' .
Pain in the distribution of the sciatic nerve at the back of the
leg from pressure on the roots contributing to the nerve.
(3) GOUT
A metabolic disease associated with a high blood uric acid,
crystals of which are deposited in joints causing recurrent
attacks of arthritis.
The high blood uric acid is usually due to an over-
production in the body, but there may be a defect in renal
tubular excretion in addition. The over-production is a result
of abnormal purine metabolism - purines are proteins present
in many body cells, especially those of the pancreas and liver.
Inherited as a dominant, gout is 95070 a male disease, and
usually presents after the age of 50. There are racial predis-
positions, a high uric acid being common in Pacific islanders.
Symptoms and signs

Recurrent attacks of pain and inflammation in one or more
joints.
Metatarsophalangeal joint of the big toe is commonly
affected.
Symptoms characteristically come on during the night, but
may be precipitated by a heavy meal or alcohol, or by an
infection or operation.
The pain may be excruciating.
The joint is swollen, red and shiny and exquisitely tender.
Deposits of uric acid may also be seen as white 'tophi' under
the skin, especially at the cartilage of the ears.
(4) ANKYLOSING SPONDYLITIS

An inflammatory disease of the joints of the spine, affecting
young men. Its cause is unknown but most patients have the
HLA group B27.
Symptoms and signs

Occur before the age of 30 and the condition should be
suspected in a previously healthy man complaining of back-
ache or pains in the thighs.
The sacroiliac joints are first affected.
Changes are seen on X-ray.
The ESR is raised.
Pain and stiffness of movement of the lumbar spine, spreading
up to involve dorsal and even cervical spine.
In later stages bony fixation (ankylosis) of the joints occurs
and the patient has a rigid 'poker-back' or 'bamboo spine'.
(5) FIBROSITIS
The term rheumatism is popularly used to mean aches, pains
and stiffness attributed to disorders in joints, ligaments or
muscles. Inflammatory disease of muscles is not, however, a
common cause of recurrent symptoms - the only common
inflammation or infection is epidemic myalgia or Bornholm
disease, caused by a Coxsackie virus, presenting as chest wall
pain and tenderness, and settling within a week or 10 days.
Abscesses of muscles may occur in the tropics. Myositis may
occur in the rare connective tissue diseases.
When a patient complains of 'rheumatism' or 'fibrositis', it
is important to exclude conditions such as the chronic
rheumatic disorders, local post-traumatic conditions such as

frozen shoulder (inflammation of the tendons and capsule of
the shoulder joint), polymyalgia rheumatica and bone
disorders. Osteoarthritis of the spine is a common cause of
many 'rheumatic' pains. Muscle spasm, from nerve irritation
or in an attempt to protect the joint from undue movement,
may explain some of the aches and tenderness around the part,
and the symptoms are ascribed to the muscles instead of to the
causative disease.
The occurrence of symptoms is often ascribed to undue
strain, or exposure to draughts, cold and dampness, and a
warm climate may improve them. Symptoms are worse in
those who are depressed - depressive illness may present with
rheumatic pains.
(6) CONNECTIVE TISSUE ('COLLAGEN VASCULAR')

DISEASES
A group of diseases in which there is degeneration of
connective tissue in association with inflammation of small
blood vessels. They may be disturbances of the immune
mechanism of the body, and abnormal globulins and anti-
bodies may be detectable in the blood, with a raised ESR.
(a) SYSTEMIC (DISSEMINATED) LUPUS

ERYTHEMATOSUS
This relatively rare condition occurs in young women. The
cause is unknown but many tissues are involved, possibly from
deposition of immune complexes in the small arteries supply-
ing them, with resultant inflammation and degeneration. The
condition gets its name from an erythematous rash across the
nose and cheeks, a 'butterfly' distribution.
Symptoms and signs

General symptoms include fever and malaise.
Polyarthritis, similar in distribution to rheumatoid arthritis,
but more transient.
'Butterfly' erythema at nose and cheeks may be present, often
mild but worsened by exposure to sunlight.
Erythema at the nail bases, due to dilated small vessels
(telangiectasis), is characteristic.
Purpura may occur.
Thrombosis in small arteries may cause cold, pale fingertips
with gangrenous patches.
Acute glomerulonephritis and the risk of renal failure may
occur or the more chronic picture of nephrotic syndrome with
albuminuria and oedema.
The pleura may be involved, with pleurisy and effusion.
A tendency to haemolytic anaemia.
Increased drug sensitivity with rashes.
Investigations
The white cell count is low, LE latex and antinuclear antibody
(ANA) tests in the blood are useful in screening and the DNA
binding test (for anti-DNA antibodies) is almost specific.
(These tests detect the abnormal antibody in the blood which
affects the white cells, some of which engulf others and appear
as the typical LE cells on a blood smear.)
ESR is high.
Blood urea may be raised.
(b) POL YARTERITIS NODOSA AND CRANIAL

ARTERITIS
Polyarteritis nodosa is a rare disturbance of small arteries
throughout the body, commoner in middle-aged men.
Symptoms and signs

Fever.
Tendency to arterial thrombosis with nodulation related to
arteries.
Peripheral neuritis.
Raised white cell count with many eosinophilic cells.
High ESR.
May be a patchy recurrent pneumonia.
The diagnosis may be confirmed by muscle biopsy, the blood
vessels in the muscle showing characteristic changes.
Structure of bone
Bone contains living cells, in a protein matrix in which calcium
salts are deposited. Flat bones such as the sternum, vertebrae
and pelvis contain active marrow concerned in blood
formation. However, even the long bones are not simply
supporting structures, they are metabolically active, calcium
deposition and resorption occurring all the time.
Rarefaction of bones occurs in osteoporosis, osteomalacia,
hyperparathyroidism, myelomatosis and in metastatic bone
disease.
(7) OSTEOPOROSIS
Osteoporosis is a thinning of the bones, a loss of bone density.
Normal stresses and strains protect against it, and if a limb is
immobilized, osteoporosis occurs. Thus it may be seen locally
in the bones round splinted joints, but occurs more generally if
a patient is confined to bed. Post-menopausally, it may be due
to urinary calcium losses from hormonal deficiency.
Osteoporosis is very common in the elderly. The cause is
uncertain. There seems to be a fall in calcium absorption after
the age of 70 (possibly due to mild vitamin D deficiency). The
hormone calcitonin (secreted mainly in the thyroid and
concerned in maintaining the calcium content of the bones)
may playa part in osteoporosis.
Symptoms and signs

Osteoporosis especially affects the spine, the vertebrae
becoming smaller, so that elderly people do become shorter in
stature and may have prominent transverse skin-creases across
the abdomen.
There are aches and pains in the back.

Fracture of the neck of the femur, a common result of a fall in
the elderly, may be more liable to occur if there is osteoporosis.
(8) METASTATIC BONE DISEASE

Malignant secondary deposits (metastases) are a common
cause of bone disease. Bone aches and pains occur - symptoms
may precede those of the primary tumour. X-ray changes are
late, but bone scanning using radioactive isotopes may allow
earlier detection. Spontaneous 'pathological' fractures may
occur, and in the spine these may cause cord compression and
paraplegia.
The primary site may be in the prostate, breast, thyroid or
lung.
(9) DISEASES OF MUSCLE - MYOPATHY

fa} THE MUSCULAR DYSTROPHY GROUP (INHERITED
MYOPATHIES)
This is a group of rare, hereditary disorders affecting mainly
young people, and causing muscular weakness.
Types
Duchenne type - pseudohypertrophic muscular dystrophy.
Presents in infancy, occurs only in boys - it is a sex-linked
recessive disorder. Waddling gait, weakness and tendency to
contractures, muscles appear bulky but become progressively
paralysed - child rises from the floor by 'climbing stairs' -
and progressively weaker over 10-20 years.
Limb-girdle type - adolescents affected, both sexes,
autosomal recessive, weakness of shoulder and in raising arms,
difficulty climbing stairs - progressively weaker over 10-20
years.
Facio-scapulo-humeral type - less severe and may present in
adults - autosomal dominant inheritance so that affected
individuals pass it on to half their children. Weakness of facial
muscles and difficulty in closing the eyes and puffing the
DIFFERENTIAL DIAGNOSIS OF JOINT PAINS

Site, onset and duration Pre-existing symptoms
or conditions
Rheumatoid small joints affected, gradual commoner in females, pre-

arthritis and continual deterioration, dominantly develops in
permanent, crippling 30-40-year-olds; bouts of
fever, fatigue, anorexia
Osteoarthritis larger weight-bearing joints, overweight and elderly; no

continual restriction of systemic upset
mobility
Gout usually an isolated joint predominantly male adults,

affected - big toe com- may be precipitated by
monest; worse at night; alcohol
recurrent attacks with
remissions
Septic arthritis any joint, follows systemic pyogenic, tuberculous or

disease or injury; resolution gonococcal infection
depending on extent of precedes; fever, anorexia,
local destruction malaise
Traumatic any joint, recovery depends history of trauma, rapid

arthritis on extent of injury development with 24 h of
symptoms; no systemic upset
morning stiffness, rheumatic nodules, anaemia, Rh factor present, high ESR,

joint deformity and inflammation WBC raised, X-ray shows joint
deformity and osteoporosis
continual joint movement restriction; X-rays show bone deformity, os teo-

swelling of joint, non-inflammatory phytes, destruction of articular surface;
ESR normal
'tophic' deposits in ear cartilage; swollen raised serum uric acid, abnormal purine
red joint extremely painful to touch or metabolism results, uric acid crystals in
movement joint aspirate
all movement painful, single red swollen cytology and culture of aspirate confirms
joint causative organism; ESR, WBC raised;
may be proteinuria
swollen joint, loss of movement, pain blood tests normal, X-ray may show
increases after initial injury fracture or, under stress, ligament tear
cheeks, winging of scapulae, some weakness in arms and legs

with tendency to waddling gait. Often remains in this mild
form over many years.
Investigations
Serum enzymes - creatine kinase raised in Duchenne type.
Electromyography - investigation of electrical activity of the
muscles, which is disturbed.
Muscle biopsy.
(b) ENDOCRINE, METABOLIC AND CARCINOMATOUS

MYOPATHIES
Proximal myopathy, weakness of the muscles of the shoulder-
girdle and thigh, may complicate thyroid disorders (thyro-
toxicosis, myxoedema). The patient has difficulty in raising
the arms above the head, and in stair climbing. There may be
wasting of the affected muscles.
A low serum potassium level (hypokalaemia) causes
muscular weakness, and occurs in aldosteronism, but the
excessive use of diuretics is the commonest reason.
Rare defects of muscle sugars and enzyme abnormalities are
associated with muscle weakness.
Carcinoma, especially bronchogenic carcinoma, may be
associated with myasthenia-like muscle weakness and should
be considered in the middle-aged and elderly.
(10) MYASTHENIA GRAVIS

An uncommon disease with onset in adult life or late child-
hood. There is a defect in the transmission of the nerve impulse
at the neuromuscular junction so that the muscle fails to
contract and remains flaccid.
The disease is due to destruction of the acetylcholine
receptors at the neuromuscular junction and antibodies to this
receptor are demonstrable in the blood - thus it is an
autoimmune disease. The disturbance of immunity may be
related to a defective thymus gland, which may be enlarged or,
in some cases, contain a tumour.
Symptoms and signs
The patient experiences muscle weakness, especially of
muscles of the face, so that he may have difficulty in keeping
his eyes open, in chewing, and even in swallowing.
The arms may also be affected.
Symptoms are worse towards the end of the day when the
muscles are tired.
Diagnosis and treatment

The diagnosis is confirmed by the slow intravenous injection
of edrophonium 10 mg, a cholinergic drug which produces an
immediate return of muscular power.
Plasmaphoresis, a technique of filtering the blood plasma to
remove the acetylcholine receptor antibody, is diagnostic.
Chapter 10
The Skin
Disorders of the skin are common, a frequent cause of consult-

ation but an infrequent cause of hospitalization and an excep-
tionally rare cause of death. Acute and chronic infections,
eczema, dermatitis, allergic rashes and the rare skin tumour
are the main disorders and more than 15070 of the population,
in all age groups, will seek medical attention in each year.
Diagnosis of disorder will depend on symptoms, signs,

observation of the patient (particularly) and examination of:
(A) the skin,
(B) blood tests,
(C) urine tests,
(D) biopsy.

(1) a localized, or generalized, rash,
(2) swelling,
(3) pain,
(4) itching.
185
Common Disorders of the Skin

(1) INFECTIONS
(a) BACTERIAL
Boils are due to staphylococcal infection in a hair follicle and
may go on to abscess or carbuncle formation.
Impetigo is an infection caused by staphylococci and strep-
tococci together, and consists of blisters, tending to become
pustular and crusted, on inflamed skin. It may follow neglect,
scratching and lack of cleanliness after abrasions or septic
spots, and is seen mainly in children.
Erysipelas is a spreading inflammation in the superficial layers
of the skin near a mucocutaneous junction such as the lips or
nose. It is a streptococcal infection.
Cellulitis is a spreading inflammation in the subcutaneous
tissues from a septic area or ulcer. The cause is usually a
staphylococcal or streptococcal infection.
(b) FUNGUS
Infection of the mouth with the fungus Candida (Monilia)
results in the white patches called thrush, which is found in
debilitated patients or those receiving broad-spectrum anti-
biotics. A similar infection may occur in the vagina, causing
pruritus vulvae, and is especially likely to occur in diabetics
and women using oral contraceptives.
Intertrigo is a moist red rash occurring where two surfaces rub
together and cleanliness is lacking, and may be due to an
eczema reaction complicated by a low-grade infection with a
fungus of the Candida group. It is common under the breasts
of obese women - there is an offensive oozing patch with a red
edge containing pinpoint vesicles.
Tinea is a term applied to other human fungus infections of the
skin; conditions sometimes called ringworm. In children,
ringworm may affect the hair; but in adults the condition is
seen in moist areas - between the toes (athlete's foot) and at the
groins. Between the toes the skin becomes soggy and
THE SKIN 187
macerated. At the groins there is a spreading red ring (which
gives the disease its name) of inflammation, with healing
tending to occur in the centre of the patch - the same appear-
ance as intertrigo, with considerable irritation and some
odour. Tinea can also affect the nails. Other forms of ring-
worm are acquired from contact with infected animals.
(e) VIRUS
Herpes simplex is a virus infection, causing 'cold sores' around
the lips and nose, sometimes in association with lobar
pneumonia. It may also attack the genital area.
Herpes zoster (shingles) is a vesicular eruption along the line of
a nerve - seen usually on the trunk, sometimes in the face from
involvement of the ophthalmic division of the fifth cranial
(trigeminal) nerve. Pain may be severe, with tendency to
secondary infection. The virus responsible also causes chicken-
pox, yet contact spread is rare.
Molluscum contagiosum is a virus infection causing little water
blisters; it may be acquired at swimming pools.
Common warts are induced by virus infection, though the
reasons for their appearances and disappearances are obscure.
(2) INFESTATIONS
(a) LOUSE INFESTATION (PEDICULOSIS)
Lice are small flat insects which feed on blood. Head lice may
infest the scalp of children, young women and youths with
long hair, the eggs or nits being attached to the shaft of the
hair. The nits are greyish-white specks and in severe infestation
the hair may be covered with them. The irritation of the adult
lice causes scratching and minor skin infection, with enlarge-
ment of the occipital and cervical lymph glands as a result.
Infestation spreads easily in schools.
Body lice affect people who are dirty - vagrants, and those
living in squalid conditions. The bites appear as small red
spots, and there is much scratching and slight secondary
infection. The louse lives in the seams of clothing, where it lays

its eggs.
Crab lice affect the pubic region and are spread by sexual
intercourse.
(b) SCABIES
Scabies is an infestation with a small mite called the acarus.
The female acarus is just visible to the naked eye and burrows
into the epidermis, causing severe itching. Favourite sites are
the clefts of the fingers, the front of the wrists and elbows,
axillary fold and pectoral region - areas which can be
scratched, the parasite being spread by the fingernails. The
burrows are visible as greyish lines up to a centimetre in length
and there may be a raised red eruption which tends to second-
ary infection. Minor epidemics of scabies occur in school-
children and in the elderly in hospital, the condition being very
contagious in institutions. The acarus can be picked out with a
pin and identified under the microscope.
(e) FLEAS
Flea bites cause itchy raised red spots with a central bite-mark.
(3) DERMATITIS AND ECZEMA

Dermatitis means inflammation of the skin and includes the
'eczema reaction' which typically starts with erythema
(reddening) followed by the formation of tiny fluid-containing
vesicles and 'weeping' followed by a more chronic scaling stage
when the skin may become thickened or 'lichenified'.
Eczematous lesions are usually extremely itchy. The terms
dermatitis and eczema are sometimes used interchangeably.
Eczema may be present in infancy and be followed by
flexural eczema in childhood. There is an association with
asthma, and such patients are said to manifest atopy, an
inherited tendency to show hypersensitivity or allergic
reactions. The eczema and asthma may improve in adoles-
cence, but the skin seems to remain very sensitive. People with
no previous allergic history may also have skins which are
THE SKIN 189
prone to show the eczema reaction. Chemicals and drugs cause
contact dermatitis in susceptible subjects. Soaps and
detergents, and substances met with at work (occupational or
industrial dermatitis) may cause contact dermatitis.
Some patients are prone to a form of eczema, called
seborrhoeic eczema or seborrhoeic dermatitis, occurring
especially in flexures, e.g. behind the ears causing fissuring, in
the axillae, groins or under the breasts. Seborrhoea means
increased sebum and there is an association with dandruff and
dermatitis near the hair follicles.
(4) DRUG RASHES

These are very common and while the eruption may follow
local application or contact, usually it is due to a drug that has
been taken by mouth. Drug eruptions are a result of a delayed
hypersensitivity, a cell-mediated allergic reaction.
Barbiturates, especially phenobarbitone, may provoke a
diffuse blotchy-red itchy rash, or many red spots tending to
coalesce rather like measles.
Aspirin, sulphonamides, antibiotics especially ampicillin,
and oral anticoagulants such as phenindione may cause a skin
eruption in sensitive subjects.
Iodine-containing substances, used in X-ray contrast media
and in proprietary cough treatment, may cause a characteristic
vesicular rash.
Heavy metals such as gold, used in the treatment of
rheumatoid arthritis, may cause a severe exfoliative dermatitis
(erythroderma) with generalized reddening of the skin, and
there may be extensive peeling.
(5) URTICARIA
This is the appearance of itchy red lumps in the skin, from
oedema and inflammation in the deeper layer (dermis). In
some cases the patient, using his fingernails or a match-stick,
may be able to write his name on his skin.
Some individuals have this heightened reactivity when
exposed to nervous stress, such as examinations, to a hot or
cold bath or to contact with or ingestion of substances ranging
DIFFERENTIAL DIAGNOSIS·OF SKIN RASHES

Site, onset and duration Pre-existing symptoms
or conditions
Bacteriological local, rapid development, debilitation or self-neglect,

infections often follicular or following acne, evidence of contagion,
injury; may be boil or recurrent attacks
confluent sepsis
Fungus infections oral, vaginal or intertrigo, may be using oral contra-

slow development, recurrent ceptive, antibiotics (broad-
and resistant to therapy spectrum) or diabetic; animal
contact with some tineas, or
family spread
Virus infections may be single papilloma - if viraemia, often previous

wart - or widespread signs of URTI and coryza,
viraemia typical of measles, fever, headache, anorexia,
rubella, chickenpox; herpes- photophobia; 'Koplik's' oral
specific rash on lips, as spots of measles
zoster following nerve root,
or on genitalia
Eczema flexures of limbs initially, atopics have history of

may spread; may occur where asthma, contact dermatitis
skin in contact with response caused by occupa-
'sensitizer'; worse in atopy, tional exposure; seborrhoea;
seasonally strong family history
Urticaria may be widespread, only allergic history, may be

perioral, or on 'exposed' initiated by known allergen,
skin areas; onset rapid, e.g. salicylates, foodstuff, etc.,
progreSs to wheal and or cold exposure; psychogenic
'target', spontaneous response; affects the young
resolution and female mostly
Psoriasis scalp, elbows and knees - often presents in adolescent,

may be discrete or con- genetic recessive, therefore
fluent areas elsewhere on strong family history
body
THE SKIN 191
pustular, crusted discharge, raised WBC, culture of discharge

lymphadenopathy; painful confirms organism; check for
erythema surrounds glycosuria
itches and then becomes painful to normal blood tests check for
stretching; may bleed; ringworm glycosuria; mycelium grown on culture
typical in appearance; tinea may be or seen in skin scrapings under
moist with skin flake shedding; nail microscopy
changes in some
lymphadenopathy herpes accompanies ESR raised, WBC and specific anti-

skin temperature elevation. No body changes; cytology of chickenpox
itching until crusted rash of chicken- lesions unnecessary if diagnostic rash
pox or herpes develops distribution
itching, exudative, crusting rash; eosinophilia, immunoglobulin

'typical' distribution, allergic family changes
or personal history of migraine,
urticaria, hay fever, etc.
itching, may be severe, with localized occasional immunoglobulin changes;

oedema; sometimes temporarily may show evidence of parasitic
arthritic findings infestation (intestinal)
fingernail pitting, sometimes typical microscopic pattern of biopsied

destructive small joint arthropathy; lesion; X-ray shows bilateral
non-itchy, scaly rash; improves arthropathies
with UVL
from tomatoes to drugs, or following insect bites.

Severe cases go on to 'angioneurotic oedema' when there is a
puffy oedematous swelling of the eyes and face, and the larynx
may also become swollen from oedema.
(6) PSORIASIS
A common chronic skin disease, often presenting in adoles-
cence, but it may occur at any age. It is characterized by scaly
patches on the skin. The cause is unknown but there is a
familial tendency, and although the lesions appear discrete,
there is a disturbance of function throughout the epidermis.
The scaly patches often occur over extensor surfaces such as
elbows and knees but in severe cases may be much more
diffuse. The patches are disc-sized or larger, reddish and
slightly raised, the scales producing a silvery appearance with a
white line on scraping. The condition is unsightly, with much
flaking of the scales, but there need be no itch. Psoriasis may
be associated with an arthritis rather like rheumatoid arthritis,
though the terminal joints of the fingers are more liable to be
involved and psoriasis of the nails may be associated.
(7) TUMOURS OF THE SKIN

(a) PRIMARY TUMOURS
The rodent ulcer or basal cell carcinoma is a slow-growing
tumour occurring on the face near the nose, eye or ear of an
elderly person.
A squamous cell carcinoma is a more rapidly growing malig-
nancy which spreads to lymph nodes.
The common mole or naevus rarely becomes malignant, but
the malignant melanoma is a pigmented spot of high malig-
nancy which spread locally, and metastasizes commonly to the
liver.
(b) SECONDARY TUMOURS

Secondary deposits present as little lumps in the skin, which
may ulcerate. The primary is commonly a carcinoma of the
lung or stomach. Skin involvement means that the spread is
THE SKIN 193
extensive and the outlook poor, with only palliative treatment
being possible.
Skin deposits may also occur in leukaemia and the
reticuloses.
Acanthosis nigricans is a dark scaly eruption which is a
reaction to carcinoma. The tumour may not be clinically
manifest, but the appearance of the characteristic skin
eruption should lead to a search for its presence.
Chapter 11
The Endocrine-Hormonal
System
The commonest disorder of the endocrine-hormonal

metabolic system is diabetes, with thyroid, adrenal and
pituitary disorders following in order of frequency. They
account for at least 2070 of all hospital admissions and all
increase in incidence with age.

(A) blood tests,
(B) urine tests.

(1) loss (or gain) of weight,
(2) frequency of urination,
(3) fatigue (or excitability),
(4) anorexia.
(A) BLOOD TESTS

These will be complicated, depending on the disorder being
investigated. Hormonal level estimation in blood has only
195
comparatively recently been made available through

procedures such as electrophoresis, chromatography and
radioisotope tests - although blood sugar estimation has been
practicable for many years.
(B) URINE TESTS

Assessment for glycosuria has been made for centuries - the
development of enzyme strip tests and special tablet tests has
revolutionized the more accurate measurement. Hormonal
output analysis is, nevertheless, much more complicated and
primarily an achievement of the comprehensively equipped
laboratory.
Common Disorders of the Endocrine-

Hormonal System
(1) DIABETES
Diabetes mellitus is a disorder of metabolism characterized by
a high blood sugar and the passage of large quantities of sugar-
containing urine.
Cause of diabetes mellitus

Diabetes is due to a relative or absolute deficiency of insulin
action. Insulin is the pancreatic hormone.
The pancreas has two component parts - the exocrine digestive
enzyme-secreting part, and the endocrine part, the islets of
Langerhans. Insulin is secreted into the bloodstream by the
cells of the islets. The stimulus to insulin secretion is a high
blood sugar level acting directly on the pancreas, but glucose
and amino acids in the upper intestine after a meal also
stimulate insulin secretion indirectly by the action of certain
gut hormones on the pancreas.
In diabetes, the secretion of insulin is deranged. In the severe
diabetes of the young the cells are very defective and there is a
lack of insulin production. In older diabetics, who are
frequently obese, the plasma insulin may be higher than in a
THE ENDOCRINE-HORMONAL SYSTEM 197
thin, normal person, but there is a deficiency of secretion
relative to needs.
Diabetes sometimes runs in families, but the genetic basis is not
clear and is probably multifactorial. There is some evidence of
an association with Coxsackie virus infection, but there is as
yet no proof of a virus cause in most cases.
Insulin antagonists, pituitary- or adrenal-dependent, have
been thought to be operative. The muscles of the obese may
have a metabolic block in glucose uptake (which is sidetracked
to the fat depots) which increases insulin demands. Blood
vessel abnormalities occur in diabetes, and altered permeabil-
ity of capillaries might impair insulin passage. All these factors
create an increased demand on the pancreas to produce
insulin, and while this demand may be met for many years,
ultimately it results in pancreatic exhaustion and clinical
diabetes.
Insulin is necessary for glucose and amino acids to cross cell
membranes; where it is deficient, the body cells cannot
properly utilize carbohydrates, fats and proteins. The upset in
carbohydrate metabolism is the obvious manifestation, with
high blood glucose and glycosuria, but it is only one aspect of a
profound metabolic disturbance.
Incidence
The highest recorded population incidence is 40070 in the Pima

Indians in Arizona aged 45 or older, and there is a high incid-
ence of a type of diabetes in West Africa. Generally, there is an
association of diabetes with high calorie intake and obesity.
Clinical diabetes exists in about 2% of the population of the
UK and USA.
Diabetes is rare in infancy, quite common in childhood and
adolescence in both sexes, but most commonly presents in
patients beyond middle-age, especially women.
Clinical types
Type 1
Juvenile, growth-onset, ketotic, 'insulin-dependent' group.
The onset is in childhood or young adult life, symptoms are

severe and often acute, the patients are thin, lose weight and
are prone to ketoacidosis (excess production of ketone bodies
such as acetone and acids from fat breakdown) and coma.
Type 2
Maturity-onset, adult, non-ketotic, 'non-insulin-dependent'
group. These are middle-aged or elderly people, commonly
women, who are or have been obese. The clinical symptoms
may be mild, the condition often presenting as a diabetic
'complication' such as a septic foot sore, and ketosis is
unusual.
At some time the unduly large food intake of these patients
caused pancreatic stimulation and plenty of insulin was
produced, but ultimately the pancreas cannot quite keep up
with the demand, and symptoms result. In a proportion of
patients the pancreas may remain unable to produce quite
enough insulin, but responds to stimulation with an oral
sulphonylurea drug such as chlorpropamide.
Symptoms and signs

The diabetic patient cannot utilize glucose. It therefore builds
up in the bloodstream (hyperglycaemia), and is excreted in the
urine.
Polyuria.
The excessive water loss causes severe thirst, and dehydration

if the patient does not slake his thirst.
There is loss of weight despite a good appetite, and muscular
weakness.
In the severe diabetes of the young, the body breaks down fats
instead of sugar in an attempt to maintain energy processes.
These breakdown products are the 'ketone bodies' acetone
and keto-acids, which build up in the blood (and spill into the
urine) and are toxic to the brain. Ketosis or keto-acidosis is one
form of acidosis.
The patient becomes drowsy and ill, with vomiting,
dehydration, and air-hunger; his breath also smelling of
acetone.
Diabetic coma may occur.
Complications
Vascular disease
Diabetics are prone to develop arteriosclerosis (atheroscler-
osis), the degenerative disease of the lining of the arteries,
related probably to the disturbed lipid (fat) metabolism. There
is a raised incidence of coronary and cerebral arterial disease,
and involvement of the leg arteries is very common - including
symptoms such as intermittent claudication - but the distal
arteries may be more affected, leading to gangrene of the toes
and feet.
Eye disease
Retinopathy is the most serious ocular complication of
diabetes, and the single most common cause of blindness
among the middle-aged. Some years after the diagnosis of
diabetes, little aneurysms and haemorrhages related to the
retinal capillaries and veins become visible with the
ophthalmoscope, and sometimes 'exudates' are seen. These
may involve an important part of the retina, causing visual
impairment.
Renal disease
There are capillary changes in the renal glomeruli where they
become abnormally permeable resulting in proteinuria,
usually slight, but occasionally severe, with nephrotic
syndrome and oedema, progressing to renal destruction and
uraemia.
Neuropathy
Peripheral neuritis or neuropathy may occur in poorly
controlled diabetes, with pains and paraesthesiae (pins and
needles) and sensory loss; the patient may burn or injure his
feet without being aware of it. There is loss of vibration
sensation, loss of ankle and knee jerks; there may be muscular
weakness.
Infections
Pruritus and vulval irritation are due to infection with the
fungus Candida (Monilia) albicans, thrush, which may feed on
the sugar deposited from the urine.
Skin sepsis and carbuncles, often staphylococcal, are
common.
THE DIAGNOSIS OF DIABETES - URINE AND BLOOD

TESTS
Glucose
(a) Qualitative tests. Clinistix, Tes-tape, and compound strips
such as Multistix - the test area on these strips is specific for
glucose.
(b) Quantitative tests. Clinitest tablets are based on the same
principle. Having established the presence of glucose with a
preliminary strip test, the Clinitest test allows an estimation of
its quantity, thus:
orange-red, 2070 - urine full of sugar
yellow-brown, 1% - considerable sugar
green, Y2% - slight sugar
blue, nil - no sugar.
In the management of diabetes, it is important to test
specimens freshly produced by the kidneys and corresponding
to the blood at the time; thus a true 'morning urine' is obtained
by voiding the bladder on wakening and discarding this urine
(which has lain in the bladder all night), then passing a fresh
specimen Vz-l h later for test.
Ketones are detected by the Acetest tablet or Ketostix strip.
In severe diabetes the urine, though pale, is of high specific
gravity from its glucose content.
Blood tests
The terms blood sugar and blood glucose are synonymous.

In health the fasting blood glucose is less than 5.5 mmolll
(100mg/dl) and even after food seldom rises about 6.7 mmolll
(120 mg/ dl). In most people glucose does not appear in the
urine until the blood glucose is over 1O.0mmolll (180mg/dl),
the renal threshold for glucose. Some normal people have a
low renal threshold and a 'renal leak' for glucose - renal
glycosuria. In the elderly, the renal threshold may be raised.
In the presence of other clinical signs, a casual blood glucose
level of over 10 mmolll (180 mg/ dl) confirms the diagnosis of
diabetes without need for further tests.
In doubtful cases a glucose tolerance test is carried out. The
patient takes his meals normally the day before, but has
nothing to eat on the morning of the tests. A fasting blood
glucose specimen is taken then 75 g of glucose or the equivalent
quantity of liquid glucose is drunk in 5 min in 200-500 ml of
flavoured water. Further specimens for glucose estimation are
taken after Yz h, 1 hand 2 h. In diabetes the fasting blood
glucose level is usually raised and the subsequent levels which
can be plotted as a graph or 'curve', rise very high, sometimes
up to 20 mmolll (360 mg/dl), and fail to return to the fasting
level in 2 h as in the normal. The diagnosis of diabetes is made
if the fasting blood glucose concentration is 7 mmolll
(126 mg/ dl) or over, or the 2 h level is 10 mmolll (180 mg/ dl) or
over.
The Dextrostix strip test is a most useful screening test of the
blood glucose level: a drop of blood is placed on the test area,
washed off after a minute, and the grey colour compared with
225
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"Ol 150
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125 ~
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Glucose tolerance curves of diabetic and non-diabetic

a set of standards. The range for visual estimation is

0-14 mmolll (250 mg/ dl). It is difficult to be accurate at the
higher levels with the naked eye, but portable instruments such
as a reflectance meter are available.
ACUTE COMPLICA TlONS OF DIABETES

(i) Hypoglycaemia
This is really a complication of therapy, too much insulin

causing an excessive drop in the blood glucose level.
Symptoms and signs

The onset may follow unaccustomed exertion or activity, or a
missed meal.
There is sudden weakness, unsteadiness, dizzy feelings, with
tremulousness and sweating from outpouring of adrenaline as
the body attempts to raise the blood glucose by breaking down
liver glycogen.
The patient may become dis orientated and violent before
collapsing in coma.
(ii) Diabetic ketoacidosis (ketosis) and coma
Diabetic ketosis is a condition of gradual onset, though a

young diabetic may present in this way. In a known diabetic,
ketosis follows a period of inadequate insulin dosage, and this
may have followed infection or stress, which create an
increased insulin requirement.
Symptoms and signs

The patient is dehydrated and thirsty, the tongue is dry.
Often there is abdominal pain simulating appendicitis or an
'acute abdomen', and vomiting.
The breathing is deep and sighing (air hunger) in an attempt to
excrete the acids as carbon dioxide from the lungs.
The blood pressure falls.
The level of consciousness deteriorates with coma.
There will have been a stage of polyuria, though oliguria may
have followed.
The urine is full of glucose and ketones.
(2) THYROID DISORDERS

The thyroid gland consists of a left and right lobe lying against
the lower half of the thyroid cartilage, united by a isthmus
across the front of the trachea. It secretes the iodine-containing
hormone, thyroxine, a metabolic stimulant acting on many
tissues.
(a) SIMPLE GOITRE
This may be due to iodine deficiency in endemic areas; the

addition of tiny quantities of iodine to salt is preventive.
However, simple goitre is not always due to iodine deficiency
and may have a genetic basis. Slight thyroid enlargement is
common in pregnancy, related to increased iodine demands.
Simple goitre is a soft swelling of the thyroid gland and is
commonest in young women. It may be regarded as an attempt
by the thyroid to produce enough of its hormone secretion by
enlarging.
(b) THYROTOXICOSIS - HYPERTHYROIDISM

('GRAVES' DISEASE') - TOXIC
GOITRE
This is overactivity of the thyroid gland, the excess thyroxine
causing increased metabolism. Thyrotoxicosis may be a
disturbance of the immune mechanism, an autoimmune
disease.
Thyrotoxicosis is commoner in women and there is a
familial tendency.
Symptoms and signs

The patient complains of excitability, 'nerves' and irritability
and may notice that she loses her temper more easily than
before.
She feels the heat badly and prefers cold weather.
The palms are warm and sweaty and there is a tremor of the
fingers.
The pulse is rapid.
The appetite remains good, the patient may say that she 'eats
like a horse', but there is loss of weight from the increased
metabolism.
With the stethoscope a 'bruit' may be audible over an enlarged
thyroid, from the increased blood flow.
There is a varying degree of 'exophthalmos'. Exophthalmos is
protrusion of the eyeball, but the term is used to describe
prominence of the eyes. The commonest sign is a 'staring'
appearance from overactivity of the sympathetic nervous
system which supplies a small muscle in the upper lid, causing
lid retraction. There is 'lid lag' on eye movement so that more
of the white sclera is seen and the eyes appear prominent.
Investigations
The diagnosis is confirmed by:
(1) Clinical features such as weight loss and raised sleeping
pulse.
(2) Raised T4, corresponding to thyroxine, and estimated by
radioimmunoassay in the blood.
(3) TRH test - an injection of TRH normally releases TSH
(thyroid stimulating hormone) from the pituitary but in
thyrotoxicosis the TSH is already suppressed by the high
thyroid activity and the blood level does not rise.
(4) High uptake of radioactive iodine (131 1 or 125 1) over the
thyroid gland.
(c) MYXOEDEMA - HYPOTHYROIDISM-

UNDERACTIVITY OF THE THYROID GLAND
In the newborn baby the thyroid gland may function
defectively or be absent. Early diagnosis is essential and
screening tests at birth for blood thyroxine or TSH levels are
necessary.
In adults hypothyroidism usually follows destruction of the
thyroid gland by an autoimmune process, and antibodies are
detectable in the blood. At some stage there may have been
swelling and lymphocyte infiltration of the thyroid -
(Hashimoto's disease); the condition ends up as atrophy, with
complete lack of thyroxine, and the clinical picture called
myxoedema.
Symptoms and signs

The condition is commonest in middle-aged women.
As the thyroid fails to produce enough thyroxine, the bodily
functions generally run down.
The patient loses interest in life and becomes slower with
coarsening and puffiness of the facial appearance and skin.
Characteristically slow relaxation of the tendon reflexes.
Patients become increasingly sluggish, have a husky voice and
feel the cold badly.
The pulse is slow, and there may be pericardial effusion.
Investigations
The diagnosis is confirmed by a low blood thyroid index and a
raised TSH (thyroid stimulating hormone, from compen-
satory pituitary activity). Thyroid antibodies may be detected.
The serum cholesterol is high.
(3) PARATHYROID DISORDERS

These four glands, situated behind the thyroid, control
calcium and phosphorus metabolism, preserving the normal
blood calcium level. Excess parathyroid hormone raises the
blood calcium by action on kidneys and bones.
(A) HYPOPARATHYROIDISM
This may occur spontaneously or following inadvertent
removal of the parathyroids at thyroid operation.
Symptoms and signs

The blood calcium falls, causing increased irritability of nerves
with painful muscle cramps and spasm-tetany.
There is painful flexion of the wrists with metacarpophal-
angeal joints, with extension of the fingers.
There may also be spasm of the larynx.
Tapping over the facial nerve produces twitching of the facial
muscles.
Tetany may be provoked by over-breathing, leading to loss of
carbon dioxide and tendency to alkalosis.
(B) HYPERPARA THYROIDISM
Overactivity is usually due to a benign tumour of one "para-

thyroid gland. It is rarely palpable. Radioisotope scan (using
labelled methionine) may aid in its location.
Symptoms and signs

In severe cases, calcium is dissolved from the bones, producing
osteitis fibrosa cystica, and fractures.
Calcium is high in the blood and urine, and may be deposited
in the kidneys and cause renal calculi.
There is often polyuria.
Raised serum calcium.
(4) ADRENAL GLAND DISORDERS

The adrenal or suprarenal glands are situated one on top of
each kidney. The adrenal gland has a cortex, essential to life,
and a medulla which functions independently producing
adrenaline-like hormones. The cortex produces three groups
of hormones:
(1) Hydrocortisone (cortisol) - a glucocorticoid - so called

because it increases protein breakdown resulting in
increased production of glucose; essential for normal
response to stress and injury; also has sodium-retaining
action.
(2) Aldosterone, concerned in sodium and water balance
through its action on the renal tubule. Causes sodium
retention.
(3) Sex hormones, which are dominantly masculinizing
(androgenic) even in women.
(a) OVERACTION
(i) Overproduction of cortisol
This is usually due to pituitary overactivity, with excessive

production of ACTH which causes bilateral adrenal enlarge-
ment and overproduction of cortisol.
Symptoms and signs

There is 'mooning' of the face which is often high-coloured.
Obesity of the trunk with thinning of arms and legs.
Muscular weakness.
Thinning of the skin with easy bruising.
Thinning of the bones causing osteoporosis and sometimes
fractures.
Hypertension and diabetes mellitus.
Investigations
The diagnosis is confirmed by raised urinary and blood
cortisol levels throughout the 24 h (blood levels are normally
lower late at night), and raised ACTH (estimated by radio-
immunoassay) if there is primary pituitary overactivity.
(ij) Aldosteronism
Primary aldosteronism is due to a tumour, usually benign,
producing excess aldosterone, causing hypertension, weakness
and polyuria. The serum potassium is low, and the blood
shows a tendency to alkalosis.
Secondary aldosteronism occurs when there is a threat of a
lowered plasma volume, as in nephrotic syndrome and

cirrhosis of the liver; it may also occur in congestive cardiac
failure. It results in salt and water retention with increased
oedema.
(iii) Adrenal virilism
This is due to inappropriate production of masculinizing sex

hormone by the adrenal cortex. It may cause precocious
puberty, or difficulties in sexual designation of infants who are
really female but appear male. Cases in adults are usually due
to malignant tumours of the adrenal.
The urine contains an excess of hormone breakdown
products, measured as 17-ketosteroids (oxosteroids).
(b) UNDERACTION
Addison's disease
This is a result of deficiency of cortisol and aldosterone.
Symptoms and signs

Loss of appetite and of weight.
Vomiting.
Low blood pressure.
There is a brown pigmentation of the skin, well seen in flexures
(e.g. axilla) and scars and in the forehead at the hair line. (The
cortisol deficiency causes an increased secretion of ACTH by
the pituitary and this is associated with increased secretion of
MSH, a hormone which stimulates the production of the
melanin pigment.)
There is progressive weakness, with poor resistance to stress
and infection.
Investigations
The serum sodium may be low and the potassium and blood
urea raised.
Plasma cortisol assessment is necessary.
Patients with underactivity of the adrenal cortex have a low
plasma cortisol level and in cases due to primary adrenal
disease, i.e. Addison's disease, it fails to rise after ACTH. The
blood is taken for test before, and Y2 h after, injection.
Side-effects of cortisone-like (corticosteroid or steroid)

drugs
Cortisol (hydrocortisone) is essential to life, and the adrenal
cortex secretes about 30-40 mg daily. More is required to cover
the stress of injury or infection. Apart from its replacement
role, cortisol (or cortisone, which is changed to cortisol in the
body) can be used pharmacologically in much bigger dosage to
treat conditions such as severe asthma and status asthmaticus,
overwhelming septicaemias, haemolytic anaemia, and disturb-
ances of immunity. But inseparable from such beneficial
action are undesirable actions which would ultimately result in
a 'moon' face, muscle weakness, thinning of the bones, hyper-
tension, tendency to diabetes and possible worsening of peptic
ulceration.
In an attempt to avoid such effects, synthetic steroids similar
to cortisol have been produced. These include prednisone and
prednisolone, 5 mg equalling 25 mg cortisone in potency.
These drugs may have less of the salt-retaining, hypertensive
properties of cortisone, but usage effects will still be seen in
long-continued dosage.
Moreover, such steroids will inhibit production of pituitary
ACTH, so that the body's own adrenal cortex becomes
atrophic, and if the administered steroid is then withdrawn,
the patient will pass into a state of adrenal cortical insuffic-
iency with hypotension and collapse.
(c) THE ADRENAL MEDULLA
Phaeochromocytoma is a tumour which secretes excess

adrenaline or noradrenaline - the hormones released at
sympathetic nerve endings.
There is hypertension, often paroxysmal, severe sweating
and pallor.
The tumour may be palpable, or detectable at IVP or on

X-ray after retroperitoneal injection of gas.
Adrenaline breakdown products (catecholamines) are
detected in a 24 h urine collection.
(5) PITUITARY GLAND DISORDERS
The pituitary is a small gland (about the size of a pea), situated

in a fossa at the base of the skull. Above it is the optic chiasma.
The pituitary stalk is connected with the hypothalamus, the
part of the brain concerned with emotion, sleep, appetite and
salt regulation, itself producing hormones which stimulate or
inhibit the release of pituitary hormones.
The pituitary gland has two parts: anterior and posterior.
fa} DISORDERS OF ANTERIOR PITUITARY

Growth hormone deficiency may arise from tumour or
spontaneously, and causes shortness of stature in children.
Acromegaly
Excessive production of growth hormone causes gigantism if it

occurs before the epiphyses of the bones have united. In
adults, it results in acromegaly. This literally means enlarge-
ment of distal tissues - hands and feet, and also the lower jaw
which becomes prominent, with coarsening of the facial
features. Some cases are due to tumour and the optic chiasma
may also be involved, causing visual field defects. Diabetes
may also be associated, as HGH is diabetogenic.
Lack of pituitary gonadotrophins causes amenorrhoea and
infertility. Lack of the gonadal hormones secondary to
gonadotrophin deficiency causes loss of sexual characteristics,
and the skin becomes fine and excessively wrinkled.
Under-activity of the anterior pituitary
Causes
This may occur after post-partum haemorrhage, but may also
arise spontaneously, or as a result of tumour or infiltration of
the anterior pituitary gland.
Symptoms and signs

There is commonly a history of failure to lactate after
pregnancy.
The periods do not return.
Sexual hair disappears.
The skin is pale yet the patient is not anaemic.
The patient is weak and hypotensive from lack of cortisol, and
there is a varying degree of hypothyroidism.
Investigations
The diagnosis is confirmed by finding low blood levels of
cortisol and thyroxine. Tests of the 'pituitary-adrenal axis'
help to localize the fault in the anterior pituitary. These include
response to ACTH, and insulin hypoglycaemia.
(b) DISORDERS OF THE POSTERIOR PITUITARY

The posterior pituitary releases the antidiuretic hormone
(ADH, vasopressin) in response to a signal from an area of the
hypothalamus sensitive to increased tonicity (osmolality) of
the blood. ADH acts on the renal tubules, causing reabsorp-
tion of water into the circulation and correcting the tonicity of
the blood - and less urine is formed.
Diabetes insipidus
This is due to lack of ADH, which may follow destruction of
the posterior pituitary by tumour, trauma, or infection (such
as encephalitis).
Symptoms and signs

The patient passes large quantities of extremely dilute urine -
specific gravity around 1000 - just like water.
There is great thirst and if fluid is withheld the patient will go to
any extreme to obtain water.
DIFFERENTIAL DIAGNOSIS - OF SPECIFIC ENDOCRINE

PROBLEMS
Onset Pre-existing conditions
Diabetes slow, gradual middle-aged or elderly (mostly

(maturity onset) female); family history
sometimes; lethargy
Diabetes rapid, may coryza or other bacterial virus
(juvenile growth proceed to infection, predominantly in
onset) coma young or adolescent; strong
family history; fatigue progres-
sive, drastic weight loss,
ketoacidosis
Hyperthyroidism may develop commoner in women, loss of
(thyrotoxicosis) Quickly or weight, may be exophthalmos;
progressively thyroid gland may be
enlarged
Hypothyroidism slow commonest in middle-aged
(myxoedema) women; lethargy; may have
goitre; intolerance to cold; may
have dyspnoea or dysphagia,
depending on size of goitre
Hyperadrenalism slow obesity, 'moon face', muscular
(Cushing's disease) weakness, plethora, lassitude;
some recent weight loss
Hypoadrenalism insidious weight loss, weakness, fatigue,

(Addison's disease) but may be anorexia; may follow previous
acute illness, sepsis or haemorrhage
Hyperpituitarism slow, particu- gigantism if during growth

larly during period, acromegaly in adult;
growth period visual field defects
Hypopituitarism slow, may be may have been severe illness
rapid following or post-partum haemorrhage;
other illness fatigue, depression, failure
to lactate; weight loss
obesity, polyuria, vascular raised random blood sugar, glycosuria,

disease, pruritis abnormal glucose tolerance test;
hyper lipaemia
polyuria, drowsiness, vomiting, glycosuria, acetonuria, blood sugar high
air-hunger, dehydration (fasting in excess of 180 mg/IOO ml,
10 mmolll)
rapid pulse even sleeping; raised T 4 and uptake of l31J;

'bruit' audible over gland; thyroxine levels high;
hyperactivity lymphocytosis
depression, loss of hair, low serum thyroxine, raised TSH

coarsening of facial features response, hypercholesterolaemia;
thyroglobin antibodies
amenorrhoea, virilism, hyper- raised urinary and serum cortisol;

tension, osteoporosis, may be raised ACTH anaemia, hypokalaemia;
diabetes; specific cutaneous X-ray skull may show pituitary fossa
pigmentation changes
low blood pressure, brown skin serum Na low, K and urea raised; low
pigmentation in flexures and plasma cortisol; X-ray of chest may show
'tanned' in both exposed and diminished cardiac size; intravenous
unexposed parts ACTH test abnormal
amenorrhoea, infertility, loss of high growth hormone levels and low
libido, skin changes; headache serum sex hormones; may be diabetic in
response to GTT
amenorrhoea, loss of pubic hair; low serum cortisol and thyroxine;
hypotension; may have diabetes hypoglycaemia; polyuria, polydipsia
insipidus if post-pituitary
involved
Chapter 12
The Nutritional System and
Acid-Base Balance
The commonest disorder of nutrition in the developed world is

obesity due to excessive food intake, and it is now held to affect
one in five of the population. In the rest of the world it is
malnutritIon due to an insufficient supply of food. Vitamin
deficiency is, however, seen in all localities due to poverty and
is, in some areas, becoming particularly more common in the
elderly. In hospital, deficiencies and disorders due to problems
with body water, electrolyte and acid-base balance in those
patients on treatment, is of increasing importance.

(A) body weight,
(B) blood tests,
(C) X-rays,
(D) urine tests,
(E) fluid input-output measurement.

215
(1) fatigue, weakness and malaise,

(2) breathlessness (exertional),
(3) skin rashes,
(4) oedema,
(5) anaemia,
(6) growth deficiency,
(7) orthopaedic disorders (e.g. osteoporosis/arthritis).
(A) BODY WEIGHT

A patient is considered overweight if weighing over 20 lb (8 kg)
more than the norm for age, sex, height and body build. Tables
(see page 61) published by life insurance companies offer
guides for adult norms. Fat normally constitutes 20070 of
total body weight, and skinfold thickness can also be assessed
(greater than 23 mm, male; or 30 mm female, over the triceps
in the upper arm). The diagnosis of obesity or gross under-
nutrition is, however, frequently obvious in the initial assess-
ment of the patient's physique.
(B) BLOOD TESTS

In vitamin deficiency and malnutrition anaemia is common.
Full blood film, count and serum assessments will be
necessary. In acid-base balance monitoring blood gases,
arterial and venous tests are necessary, as well as the electrolyte
status.
(C) X-RAYS
Osteoporosis or osteomalacia is assessed by X-ray, as is age in

the underdeveloped or malnourished child, by defining ossifi-
cation centre activity.
(D) URINE TESTS

Saturation tests for vitamin C absorption, or the detection of
excess calcium salts, may be employed. Urine measurement
and output and its concentration (specific gravity) in maintain-
ing acid-base balance, is essential. Urea and acetone content
of urine in starvation is a useful guide to diagnosis.
THE NUTRITIONAL SYSTEM 217
(E) FLUID INPUT-OUTPUT CHARTS
In all patients given i. v. fluids, for trauma, surgery or
correction of deficiency, the most scrupulous recording and
measurement of what is received, what is taken orally, and
what is excreted is necessary. The input-output chart is of as
much importance to patient therapy as the confirmatory serum
assessments.
Common Disorders of Nutrition

(1) OBESITY
(a) Most commonly caused by overeating - either an excessive
calorie intake or excessive dependence on carbohydrate
foodstuffs in the diet.
(b) Genetic and environmental. Obesity can start in childhood
and there may be a genetic basis in some children who have
inherited a greater number of adipose tissue cells than
others. However, children tend to follow the eating habits
of their parents. Thus obesity often runs in families.
(c) Disturbed calorie balance. Obese people often claim to eat
no more than their thinner fellows. Again, some people eat
a lot yet do not become fat. As the muscles of the obese are
not more efficient in their use of calories than those of the
thin, the explanation must lie in different energy expend-
iture or heat loss. Thin people increase their metabolic rate
in response to food consumption, channelling the glucose
to be utilized in muscle activity. Fat people may fail to do
this, for in association with an increased insulin
production characteristic of obesity, their glucose is
directed towards the fat depots instead. They may be
unable to generate as much heat as their thinner
colleagues, having a thermogenic defect related to their
'brown adipose tissue'. Lean people have a higher meta-
bolic response to adrenaline-like drugs. The obese are
generally less active and take less exercise than thin people
- exercise and weight loss may help to correct the
metabolic abnormalities of obesity.
Thus obesity may be due to inadequate exercise in a

modern society where physical activity at work is no longer
required, because of the use of machinery, and even the
benefits of walking to work have been removed by buses,
cars and trains. The gradual onset of obesity in middle age
is usually due to decreased energy expenditure with an
unchanged calorie intake.
(d) Endocrine. The obesity of Cushing's syndrome affects
only the trunk, the arms and legs being thin, and the skin is
thinned. The obese rarely have overt evidence of
'glandular disturbance', but as obesity often follows child-
birth or the menopause, endocrine factors playa part,
possibly through effects on hypothalamic control.
(e) Psychological. There does not seem to be a particularly
high incidence of psychiatric disturbance in obese people
attending hospitals. A proportion may be of tense and
anxious disposition and they gain solace from their worries
by overeating.
EFFECTS
Cardio vascular
There is a raised incidence of hypertension and arteriosclerotic
disease, especially ischaemic heart disease - the mechanical
burden on the heart and altered blood fats are responsible.
Strokes and renal failure are commoner in the obese. Varicose
veins, thromboembolism and pulmonary infarction are
complications.
Respiratory
The layers of fat impede ventilation, with increased tendency
to bronchitis and pneumonia, or chronic anoxia in extreme
cases.
Joints and ligaments

Backache, arthritis - especially of the knees and hips.
Metabolic
Increased incidence of diabetes, the insulin produced being
ultimately unable to cope with the demands of the great bulk of
fatty tissue. Increased tendency to gallstones and cholecystitis
from cholesterol upset.
Surgical problems
Access at operations is difficult, wound healing is impaired
with risk of incisional hernia, and post-operative pneumonia
and pulmonary infarction are commoner in the obese.
Life-expectancy
The obese have a shortened life-expectancy and, when ill, a
mortality rate some 30070 greater than that of the non-obese
suffering from the same condition.
(2) VITAMIN DEFICIENCY

A normal mixed diet provides adequate vitamins. Deficiency
can occur from:
(1) dietary lack - infants, the elderly, alcoholics and food
fads;
(2) failure of absorption - malabsorption syndrome, gastric
surgery;
(3) effects of drugs - such as folic acid deficiency due to anti-
convulsants.
(a) VITAMIN A (RETINOL)

Vitamin A is found in animal fats and dairy products, fish liver
oils and as a provitamin in carrots and tomatoes. It is
concerned in copper metabolism, is necessary for the form-
ation of visual purple in the retina and for the maintenance of
epithelial tissues including the skin and cornea.
Deficiency: causes night blindness; a serious deficiency causes
degeneration of the cornea.
(b) VITAMIN B COMPLEX

This includes vitamin Bl (aneurine, thiamine), vitamin B2
(riboflavine), pyridoxine or vitamin B6, and nicotinic acid
(nicotinamide, vitamin B7), vitamin B12 and folic acid.
Vitamins of B complex are found in meat, eggs and dairy

produce (milk is a rich source of riboflavine), and cereal germ
and bran (rich in aneurine). The vitamins form part of enzyme
systems concerned in carbohydrate metabolism. Vitamin Bl is
added to white bread.
Deficiency: isolated vitamin Bl deficiency causes wet beri-beri
- cardiac failure with oedema and warm extremities, and
neurological upset. This includes encephalopathy, cerebral
beri-beri - a confusional state plus signs of brain-stem
involvement such as nystagmus and ocular nerve palsies.
Nutritional peripheral neuritis, dry beri-beri, occurs in
alcoholics and after long illnesses associated with vomiting and
poor dietary intake.
Vitamin B2 deficiency may occur in malabsorption states
and causes cracks at the corners of the mouth (angular
cheilitis) and sore, red tongue. Such findings also occur in
nicotinic acid deficiency, which classically causes pellagra -
dermatitis, diarrhoea and dementia.
Findings such as a sore tongue or cracked lips should
indicate the possibility of vitamin B deficiency in alcoholics or
the elderly.
Pyridoxine deficiency may complicate isoniazid therapy for
tuberculosis due to metabolic interference, causing peripheral
neuritis; deficiency may also cause the rare sideroblastic
anaemia.
(e) VITAMIN 8 12
This is found in liver, meat, eggs and milk.

Deficiency: extremely rare, occurring only in Vegans, a strict
vegetarian sect who eat no animal protein whatsoever.
Pernicious anaemia is due to lack of vitamin B12 from
malabsorption following gastric atrophy and lack of intrinsic
factor, and malabsorption can also occur after gastric surgery.
(d) FOLIC ACID

This is found in liver and green vegetables, but may be
destroyed in cooking.
Deficiency: may occur in the elderly, needs are increased in
pregnancy; malabsorption may occur in intestinal disease, and
anticonvulsant drugs impair its availability for metabolism.
The result is a macrocytic anaemia, and possibly dementia in
the elderly. Pregnant women are given supplements of 100 fIg
(plus iron) to prevent deficiency.
(e) VITAMIN C (ASCORBIC ACID)
Ascorbic acid is found in fruits (e.g. blackcurrants), rose hips,

tomatoes and green vegetables. Potatoes contain some vitamin
C and as they are a staple article of Western diet they provide a
considerable part of the daily requirement. Stored potatoes
lack the vitamin, so deficiency may be seen in winter and spring
before the new crop is available. Elderly people may take little
fruit and vegetables, subsisting on tea and toast. In hospital
they are still at risk from vitamin C deficiency, for high temper-
atures and bulk cooking destroy it, and hospital food may be
deficient. Babies are born with a sufficient reserve of vitamin C
for some months and breast milk contains the vitamin. There is
little in cows' milk and it is destroyed by pasteurization.
Deficiency: results in scurvy - purpuric haemorrhages into the

skin and mucous membranes. The legs are especially affected;
other signs are scaliness of the skin around the hair follicles.
There is bleeding from the gums (and from under the
periosteum of the bones in infants), anaemia and general
debility. Wounds are slow to heal.
(f) VITAMIN 0
Natural vitamin D is vitamin D3, cholecalciferol, found in

animal fat and formed in the skin by the action of ultraviolet
light. Ultraviolet radiation of certain plant substances
produces the synthetic vitamin D2, calciferol, which has the
same action. Butter, cheese, egg-yolk and fish-liver oils are
good sources of vitamin D. Margarine is fortified with
calciferol.
Vitamin D is hydroxylated in the liver and again in the
kidney to its most active form, calcitriol. Vitamin D promotes
the absorption of calcium and phosphate from the gut and has
a direct action on bone, causing laying down of calcium salt on
the protein matrix - mineralization. Requirements are greatest
in childhood, pregnancy, and lactation; recommended daily
intake 400 units (to ug). Blood levels of hydroxy-vitamin D can
be measured.
Causes of deficiency
(1) Dietary lack in infants, and in the elderly.
(2) Malabsorption: the vitamin is fat-soluble and requires the
presence of bile salts for emulsification. Malabsorption
occurs in biliary cirrhosis and other malabsorption
syndromes.
(3) Lack of sunshine: atmospheric pollution screens off the
sun's ultraviolet rays and, since pigmented skin is less
sensitive to ultraviolet than fair skin, deficiency of vitamin
D has occurred in the infants of coloured immigrants living
in temperate or urban environments.
(4) Chronic renal disease: failure of conversion of vitamin D
to its active form.
Results of deficiency: rickets and osteomalacia

Deficiency results in rickets in children - defective calcific-
ation of the bones with swelling of the tissue at their growing
ends, impaired growth, and softening of the shafts causing
deformities such as bowing of the legs. There is muscle
weakness, abdominal distension and tetany from the low
blood calcium.
Vitamin D deficiency in adults results in osteomalacia,
demineralization and rarefaction of the bones. There are bone
pains, and trivial injury may result in fractures of the long
bones; tiny symptomless fractures may be seen on X-ray of the
pelvis, which may become grossly deformed later. There is
muscular weakness and a waddling gait. Osteomalacia may
occur in the elderly.
(g) VITAMIN E
This is contained in wheat-germ oil.
Deficiency: causes infertility in rats but this is not known to
occur in human deficiency.
(h) VITAMIN K
Vitamin K was originally found in pig-liver fat but it is also
present in the leaves of plants such as spinach and cabbage,
and in many vegetable oils. In addition, it is manufactured by
bacteria in the gut. The naturally occurring forms are vitamins
Kl and K2 which are non-toxic even when given in big doses.
Vitamin K is necessary for the production of prothrombin
and other clotting factors by the liver.
Deficiency: is unknown, but malabsorption of the vitamin
occurs in obstructive jaundice from lack of bile salts, and in
conditions such as coeliac syndrome. Deficiency may rarely
occur from the prolonged use of oral broad-spectrum anti-
biotics which alter the intestinal flora. In adults, cirrhosis of
the liver impairs prothrombin production. Oral anticoagulants
act by competing with vitamin K in the liver, blocking the
formation of prothrombin.
Prothrombin deficiency: results in a bruising tendency,
haematuria and failure of the blood to clot.
(3) MINERAL DEFICIENCIES

(a) Calcium
Milk and dairy products are rich sources of calcium. An

average diet contains 1-2 g calcium daily. Only about a tenth
of this is absorbed, balanced by a similar excretion in the urine.
Absorption is dependent on vitamin D, and is higher in
growing children where calcium is required for the bones, and
in pregnant and lactating women. Absorption is also increased
where there is excessive bone destruction and loss of calcium in
the urine as in hyperparathyroidism, where demineralization
and fractures occur if absorption does not keep pace with
demand.
Hypocalcaemia, lowering of the blood calcium, occurs in
hypoparathyroidism and to a lesser degree in vitamin D defic-
iency - rickets and osteomalacia.
States of alkalosis decrease the solubility of calcium in the

blood, so that hypocalcaemic symptoms may follow
prolonged vomiting with loss of hydrochloric acid, or over-
breathing, which washes out carbon dioxide and carbonic
acid.
Hypocalcaemia causes increased excitability of the nerves and
results in tetany.
There is a numbness and tingling in fingers, toes or around the
lips, and a characteristic spasm at the hands and feet -
carpopedal spasm.
The wrists and metacarpophalangeal joints are held in flexion,
with the fingers in extension. The sign may be provoked by
pressure on the arm with a sphygmomanometer cuff.
Tapping over the facial nerve in front of the ear elicits
twitching of the lips and muscles of the face.
There may be spasm of the muscles of the larynx, with
prolonged 'crowing' inspiration, dyspnoea and cyanosis.
Convulsions, and epileptic attacks in those predisposed to
them, may be precipitated.
Prolonged hypocalcaemia causes muscle weakness, a coarse,
dry skin, calcium deposits in the cornea, and raised intra-
cranial pressure with convulsions or precipitation of epilepsy.
Hypercalcaemia occurs in vitamin D intoxication, hyper-
parathyroidism, bone diseases such as myelomatosis, and
sometimes in carcinomatosis and sarcoidosis. Symptoms
include lassitude, anorexia, nausea, vomiting, polyuria, thirst
and renal failure follows.
(b) Magnesium
Magnesium is required in small quantities; its actions have

some similarities to those of calcium.
(c) Iron
Iron is necessary for the formation of haemoglobin. (See

Chapter 13, 'The blood and lymphatic system'.)
(d) Copper
Traces are necessary for blood formation and possibly for
nerve function.
(e) Iodine
Small quantities are necessary for normal thyroid function and
formation of the thyroid hormone thyroxine. Deficiency is one
cause of goitre, or thyroid swelling.
(f) Fluorine
A concentration of one part per million in the water supply

lowers the incidence of dental caries. Excessive doses cause
fluorosis, a hardening of the bones.
(4) ELECTROLYTE AND ACID-BASE BALANCE

DISORDERS
The body has three sources of water - the water drunk, the
water present in food, and the water formed by the metabolic
oxidation of food. Water is lost in the urine, in the faeces, and
by evaporation from the skin and exhaled air from the lungs.
The daily balance is as follows:
Water intake Water output
Water drunk 1500 ml Urine 1500 ml
Water in food 500-1000ml Faeces 100 ml
Metabolic water 200- 500 ml Skin evaporation 500ml
Lungs 400 ml
TOTAL 2.5litres
TOTAL 2.5litres
Evaporation from the skin and exhaled air represents an

obligatory litre of water per day; if the amount necessary for
adequate urinary excretion is added, then basal requirements
are about 2litres daily. Much higher intakes may be required in
hot climates and in fevers, when skin losses are greatly
increased.
Salts such as sodium chloride when dissolved in water

dissociate into particles. Thus sodium chloride dissociates into
sodium (Na) , and chloride (CI). These particles are called ions
and carry an electrical charge - hence the salts from which
they are formed are called electrolytes. Important salts or
electrolytes in the body fluids are sodium chloride, sodium
bicarbonate and potassium chloride.
The strength, tonicity or osmolality of a solution depends on
the total number of particles dissolved in it - the main
contribution is from the electrolytes.
In general terms, water will pass from a more dilute solution
on one side of a membrane to a more concentrated solution on
the other in an attempt to equalize the concentration on both
sides of the membrane - the concentrated solution exerts an
osmotic force which attracts water. The tonicity or osmolality
of the body fluids bathing the cells has to be kept constant and
equal to that inside the cells, otherwise these lose or attract
water, and break up or burst.
Sodium is the dominant ion responsible for the maintenance
of the extracellular fluid volume - that is, for the retention of
water. Potassium is the dominant intracellular ion. The cell
membrane uses energy to keep sodium out of, and to keep
potassium in, the cell. In the blood vessels the osmotic force
exerted by the plasma proteins, especially albumin, helps to
maintain the circulating fluid volume.
The volume of fluid in the body depends partly on the
stimulus of a rise in tonicity affecting a centre in the hypo-
thalamus, causing release of antidiuretic hormone and there-
fore water retention, and partly on special volume receptors in
the circulation - these may act via the kidney regulating
sodium loss. The sensation of thirst is one regulator of intake,
but the control of the body fluids is largely dependent on the
kidneys, which vary the excretion of water and salts to
maintain normality.
fa} ELECTROL YTE BALANCE

Under basal conditions very little dietary salt (sodium
chloride) is necessary, for the kidneys can, if required, secrete a
urine almost free of sodium and chloride, and no salt is lost in
the normal insensitive evaporation of water from the skin.
Thus 1-2 g salt daily is sufficient, except where losses are great,
as in visible sweating and in high fevers. Normal foods contain
little sodium, but man has developed a taste for salt, preserved
and canned meats and sausages containing large amounts.
Thus the dietary intake is very variable, from 5 g to 20 g daily
of sodium chloride, averaging 12 g which corresponds to
160 mmol sodium. This is usually much in excess of needs, the
kidneys excreting the excess.
The kidneys cannot conserve potassium - there is an
obligatory daily loss in the urine (unlike sodium). Animal and
plant cells are rich in potassium and therefore most natural
foods contain it - fruit juices are a rich source. The normal
potassium intake is about 6 g potassium chloride, equivalent to
70 mmol potassium, daily.
Sampling the blood gives an indication of the fluid and
electrolyte balance of the patient - the packed cell volume
(haematocrit), sodium, potassium and chloride being easily
estimated.
(b) ACID-BASE BALANCE

Tissue respiration results in the production of carbon dioxide,
which is duly excreted by the lung. Exercise, protein and fat
breakdown also result in the production of acids. Thus
metabolic processes are acid-forming.
The acidity of a solution is commonly expressed on the pH
scale. It should be understood that a very small change in pH
represents a big difference in concentration. Chemical
neutrality is pH 7, the pH of water. Acids have a pH lower than
7, alkalis a pH higher than 7. The pH of plasma has to be
maintained at 7.4, just on the alkaline side. Metabolic
processes would tend to shift the pH downwards, the state of
acidosis. This tendency is resisted by the presence of 'buffer
systems' in the blood which bind acids harmlessly until they
can be excreted as carbon dioxide by the lungs, or by the kidney
tubules. An important and readily measurable buffer system is
the bicarbonate system. Not only do the kidneys excrete acids,
they also reconstitute bicarbonate buffer and return it to the
bloodstream. While the urinary pH is a guide to the acidic
concentration in the body if the kidneys are working normally,

blood measurements are more accurate and are an essential
part of the management of acid-base disturbances.
A tendency for the pH to fall, that is, a state of acidosis, is
recognized by a fall in the plasma bicarbonate ('buffer base
deficit'), or a rise in the carbon dioxide. The former occurs in
diabetic ketoacidosis and renal failure, the latter in the respir-
atory acidosis of respiratory failure.
For the preservation of a normal acid-base balance, the
body needs a sufficient supply of water and electrolytes, a
normal cardiac output, and adequately functioning lungs and
kidneys.
Disturbances of Water and Electrolyte

Balance
(8) WATER DEFICIENCY
A deficiency purely of water is usually due to insufficient

intake - in desert conditions, inability to swallow, or in comas.
Water deficiency can also follow urinary losses in diabetes.
As a result, the tonicity of the extracellular fluid tends to
rise, and water moves out from the cells into the extracellular
fluid. The intracellular dehydration causes the symptom of
thirst in the conscious patient, the tongue is dry, and the urine
decreased in amount but very concentrated, of high specific
gravity.
(b) PURE SALT DEPLETION

Salt losses occur with severe sweating in the tropics and in men
doing heavy manual work in hot conditions such as foundries.
Symptoms include muscle cramps and weakness. In pure salt
depletion the sodium concentration in the plasma falls and the
urine flow might be increased to maintain it. This results in
water passing from the circulation into the cells to equalize the
osmotic pressure. Thus there is a lack of fluid in circulation
and a fall in blood pressure, but as there is cellular over-
hydration the patient is not thirsty.
In clinical practice pure water or salt deficiency states are
rare - usually the deficiency is a combined one, giving the
picture called dehydration.
(c) THE CLINICAL PICTURE OF DEHYDRATION
The clinical state of dehydration is a result of water and salt

deficiency, usually from abnormal losses. The extracellular
fluid becomes depleted but for a time plasma volume can be
maintained. Once the deficiency has reached severallitres, the
blood volume is reduced and the circulation to the kidneys
impaired, leading to acidosis and uraemia.
Causes
Insufficient intake of fluids as in coma or, more commonly,
excessive losses of fluids from the body.
Severe vomiting and diarrhoea; also paralytic ileus, a compli-
cation of intestinal obstruction of operation when fluid is
poured into the gut and lost to the circulation.
Sweating, especially in fevers in hot climates.
Polyuria in diabetes mellitus or chronic renal failure.
Severe burns - loss of serum from skin damage.
Severe haemorrhage produces pallor and collapse, a different
picture, but dehydration may be a complication, especially in
haematemesis.
Symptoms and signs

Thirst is usual, but may be absent if the deficiency is mainly of
salt.
Patient weak and lethargic.
Tongue dry.
Skin inelastic and slack, remaining in a fold when pinched up.
The eyes may be sunken.
The pulse rises, blood pressure falls.
Coma may result.
Output of urine is markedly reduced, it is concentrated (high

specific gravity) if the kidneys are healthy.
With renal failure and acidosis, there is vomiting and deep
sighing respirations - acidotic breathing, air hunger.
Observations and investigations

The nature and extent of the fluid loss, and the urine volume
must be noted - an input-output chart must be kept, plus
record of pulse, blood pressure and weight if possible.
Urine tests include specific gravity, urea and sodium concent-
ration.
Haemoglobin and haematocrit are raised in dehydration and
the blood urea may be raised. The sodium and other electrolyte
levels are a guide to therapy.
(d) OVER-HYDRATION
In health, it is almost impossible to drink too much fluid - the
kidneys will excrete the excess. Over-hydration results from
excessive intravenous fluids, especially in patients with poor
circulation and failing kidneys.
Symptoms and signs

Include lethargy, anorexia and vomiting.
Venous pressure is raised, and jugular venous pulsation may
be seen in the neck.
Fluid accumulates in the lungs, causing breathlessness and
crepitations (,moist' sounds heard with the stethoscope over
the lung bases).
Peripheral oedema develops.
Hypertension, especially in association with renal failure.
(e) OEDEMA
Oedema is due to the accumulation of excess fluid in the inter-

stitial space.
Causes
Local
(1) Increased permeability of small blood vessels as in trauma,
burns, inflammation and infection, and allergy (angio-
neurotic oedema).
(2) Lymphatic obstruction - in carcinoma and in tropical
filariasis.
(3) Venous obstruction - thrombosis, pressure of tumours.
Generalized
(1) Cardiac failure due to an excess of fluid both in the
circulation and in the tissues. Deranged volume receptors
in the circulation may act through antidiuretic hormone
secretion to cause water retention by the kidneys; in
addition, a reduced renal blood flow results in sodium
retention, and aldosterone secretion may worsen this.
Thus there is salt and water retention.
In cardiac failure the additional factor of the raised
venous pressure aggravates oedema formation in depend-
ent regions.
(2) Hypoproteinaemic states:
nephrotic syndrome,
cirrhosis of the liver,
malnutrition ('famine oedema'),
severe malabsorption.
In these conditions the plasma protein, especially albumin,
is lowered. This results in lowered plasma osmotic
pressure, the force which attracts water into solution.
When it is lowered, water passes from the blood vessels
into the tissues. The tendency for the circulating blood
volume to fall causes excess aldosterone secretion which
acts on the renal tubules to cause salt and water retention,
worsening the tissue oedema.
(3) Acute glomerulonephritis. The puffiness of the face and
peripheral oedema results from sodium and water
retention related to the renal disorder.
(4) Toxaemia of pregnancy (oedema, albuminuria, hyper-
tension and fits) has a similar basis.
(5) Corticosteroid (e.g. cortisone) overdosage, and sometimes
in Cushing's syndrome.
Clinical presentation of oedema

There is swelling on the affected part, and the skin 'pits' on
pressure with the fingertip due to the subcutaneous fluid.
Oedema accumulates in the dependent parts of the body and
where the skin is lax, ankle swelling is often the first sign.
Breathlessness from pulmonary oedema.
In the hypoproteinaemic states such as nephrotic syndrome,
and in acute glomerulonephritis, the patient can lie flat
without discomfort, so oedema may gather about the face,
hands and arms.
Effusions occur into the pleural and peritoneal cavities.
Ascites where there is a raised portal venous pressure.
(f) DISTURBANCES OF POTASSIUM BALANCE
HYPOKALAEMIA
Abnormally low serum potassium, indicates that a severe
degree of intracellular depletion has occurred.
Causes
Loss from gastrointestinal tract, especially diarrhoea, in
diseases such as cholera and severe ulcerative colitis; also
abuse of purgatives.
Renal losses and polyuria resulting from:
prolonged use of diuretics;
polyuria following acute renal failure;
use of forced diuretic therapy in aspirin poisoning.
Cardiac failure.
Cirrhosis. Potassium loss is associated with disturbed cell
function, and will be worsened by diuretic therapy unless
supplements are given.
Diabetic ketoacidosis - loss from the cells and into the urine
has occurred and in the recovery stages blood levels of
potassium may be low.
Excess aldosterone secretion and after prolonged use of
corticosteroids.
Symptoms and signs

Apathy, fatigue, confusion, muscle weakness.
Intestinal slowing and ileus (paralysis) with abdominal
distension.
Polyuria.
ECG changes, due to cardiac arrhythmias such as extra-
systoles.
HYPERKALAEMIA
Excessive potassium in the blood (normal serum potassium is
4.25 mmolll) but it need not indicate a high intracellular level.
Causes
Renal failure is the commonest cause of failure to excrete
potassium. In acute renal failure there is oliguria and as the
causative condition is usually associated with tissue damage
and release of potassium from the cells, the level in the blood
rises rapidly. In chronic renal failure the kidneys may excrete
potassium normally until the late stages, when hyperkalaemia
occurs.
Poor renal function and cellular breakdown cause hyper-
kalaemia in some cases of diabetic ketoacidosis, and states of
circulatory failure and anoxia.
The serum potassium level is raised in Addison's disease from
cortisol (hydrocortisone) lack, but the sodium deficiency is
more important.
Symptoms and signs

Muscle weakness.
ECG changes (tall T waves).
When the serum potassium reaches 7 mmolll, there is a danger
of asystole and cardiac arrest.
(g) DISTURBANCE OF ACID-BASE BALANCE
ACIDOSIS
This is a tendency for the blood to become more acid, or rather
less alkaline, than normal. The pH is lowered from its normal
7.4 but seldom falls below 7.2. The body has two routes for
getting rid of acids - the lungs losing carbon dioxide and the
kidneys excreting; the kidneys also reconstitute bicarbonate,
returning it to the circulation.
Acidosis is classified as (a) respiratory or (b) non-respiratory.
(a) Respiratory acidosis is due to impaired excretion of C02 in
respiratory failure - in conditions such as chronic bronchitis
and emphysema with superadded infection, and less
commonly in the respiratory depression of poisoning, or
following respiratory muscle paralysis (in these states anoxia is
more dominant). Thus the C02 dissolved in the blood, Pe02,
is raised above the normal 40 mmHg (5.3 kPa), the condition
called hypercapnia.
The causative condition is usually associated with dyspnoea
and cyanosis from anoxia, and the C02 retention contributes
to the restlessness, confusion, disturbance of consciousness,
and tremor.
Causes
Diabetic ketoacidosis - the ketone bodies are themselves acids.
Renal failure.
Conditions such as renal tubular acidosis, and ureteric
implantation into the colon which may impair renal tubular
function.
Conditions associated with water and salt depletion impairing
renal function, such as prolonged vomiting or diarrhoea with
loss of intestinal secretions including bicarbonate, or high
fevers with lack of fluid intake; i.e. clinical dehydration.
Cardiac arrest and circulatory failure.
Symptoms and signs

Lethargy and weakness.
Vomiting.
The raised concentration stimulates the respiratory centre
causing deep sighing respiration or 'air hunger' in an attempt
to get rid of the excess acids as carbon dioxide from the lungs.
Finally, the patient lapses into unconsciousness.
Investigations
Investigations include the blood pH and bicarbonate, which
are lowered: there is a 'base deficit'. Haemoglobin, haemato-
crit, urea, sugar and electrolytes are also measured, and Pc02.
ALKALOSIS
The blood is too alkaline, with a rise in pH. Alkalosis is not
common but may be respiratory or non-respiratory.
Causes
Respiratory alkalosis
Over-breathing with loss of C02 and carbonic acid.
Overbreathing occurs in anxiety, hysteria and occasionally
following damage to the respiratory centre in the brain stem.
In the early stages of aspirin poisoning, overbreathing is due to
stimulation of the respiratory centre by the salicylate.
Non-respiratory alkalosis
Prolonged vomiting or aspiration of gastric contents, with loss
of hydrochloric acid, as may occur in pyloric stenosis.
Excessive intake of alkalis such as sodium bicarbonate, taken
to relieve the pain of peptic ulcer.
A consequence of potassium depletion.
Symptoms and signs

Decreases the amount of calcium in the blood, causing
increased excitability of the nerves and muscles.
Paraesthesiae (tingling feelings, pins and needles).
Clouding of consciousness and convulsions.

DIFFERENTIAL DIAGNOSIS OF VITAMIN DEFICIENCY

Sources
Vitamin A animal fats, dairy produce,

fish-liver oils
Vitamin 8 complex meat, eggs, dairy produce, cereal

germ, bran
Vitamin 812 liver, meat, eggs, milk
Folic acid liver, green vegetables
Vitamin C fruits (esp. blackcurrants), green

vegetables, rose hips
Vitamin D animal fats, fish oils, dairy

produce
Vitamin E wheat-germ oil
Vitamin K pork liver, spinach, cabbage;

vegetab Ie oils
Signs of deficiency Key laboratory findings
night vision defects, corneal serum tocopherol level lowered

degeneration
beri-beri, neuropathies, cheilitis, serum levels lowered; FBC

glossitis, anaemia abnormalities
pernicious anaemia FBC abnormalities; serum levels

lowered; bone marrow changes
macrocytic anaemia FBC abnormalities; serum levels

lowered; bone marrow changes
scurvy, purpura, gingivitis, WBC ascorbate level lowered;

anaemia, debility, reduced wound saturation test response (urine)
healing
rickets in children, osteomalacia, serum calcium levels altered; X-ray

muscular weakness changes at epiphyses; serum levels
altered
none recognized none recognized
prothrombin deficiency, clotting prothrombin levels altered; bleeding

mechanism interference time extended
DIFFERENTIAL DIAGNOSIS OF ELECTROLYTE AND

ACID-BASE BALANCE DISTURBANCE
Causes
Acidosis respiratory, due to failure, chronic bronchitis,

emphysema, dyspnoea and cyanosis
diabetic ketoacidosis
renal failure
prolonged vomiting, diarrhoea
dehydration
cardiac arrest, circulatory failure
Alkalosis respiratory due to hyperventilation

salicylate poisoning
prolonged vomiting
excessive oral intake alkalis
potassium depletion
Hypokalaemia losses from GIT, e.g. severe and continual

diarrhoea
excess diuresis
renal, cardiac, liver failure
diabetic ketoacidosis
Hyperkalaemia renal failure and oliguria

hypoadrenalism (Addison's disease)
circulatory failure and anoxia
excessive intake
Symptoms and signs Key laboratory findings
lethargy, vomiting, deep sighing lowered blood pH and plasma

respiration - tremor, restlessness, bicarbonate; high Peo2
confusion; coma
increased muscular and nervous raised blood pH;

excitability, paraesthesia, con- raised plasma bicarbonate;
fusion, 'tetany', convulsions lowered Peo2
anorexia, nausea, fatigue, serum potassium lowered; urine

confusion, polyuria, intestinal potassium level lowered over
ileus, cardiac (ECG) arrhythmias 24 h if renal in origin
muscle weakness, irritability, serum potassium raised

confusion, ECG changes - asystole
and cardiac arrest
Tetany includes spasm of the fingers and muscles of the larynx,

and twitching of the face.
Investigations
The diagnosis is confirmed by the clinical history and tests such
as plasma bicarbonate and pH, and Peo2.
Chapter 13
The Blood and Lymphatic
System
The commonest disorder of the blood and lymphatic system is,

globally, anaemia. Even in the developed world where, in
general, nutritional standards are high, as many as 15070 of the
population suffer iron-deficiency anaemia. Anaemias due to
other deficiencies are the next most common disorder with
haemorrhagic diseases and the leukaemias following. These
latter, and the malignant diseases of the lymphoreticular
system, are the main cause of death from disorders of this
system.

(A) blood - red cells, white cells and serum,
(B) bone marrow and biopsy.

(1) pallor,
(2) fatigue, malaise,
(3) breathlessness,
241
(4) enlargement of the spleen and lymph glands,

(5) haemorrhages and bruising under the skin (purpura).
(A) EXAMINATION OF THE BLOOD

Blood consists of red cells, white cells and platelets suspended
in the plasma.
Red cells (erythrocytes, RBCs) are formed in the bone marrow

and contain haemoglobin, the red pigment which carries
oxygen to the tissues and removes carbon dioxide. The normal
haemoglobin is 100070 (15 g/dl), the red cell count is
5.0 x 1012 /1 (5000000/mm3). Other indices include packed
cell volume (PCV, normal 45% ), mean cell volume (MCV) and
mean corpuscular haemoglobin (MCH).
The red cell has a life of 120 days, when it is taken up and
destroyed by cells of the reticuloendothelial system in the
lymph glands, spleen and liver. The iron content of the 'haem'
is re-utilized for blood formation, the remainder goes to form
bilirubin (which becomes bile pigment), and the globin part of
the haemoglobin joins the body's protein pool.
White cells (leukocytes) are of three types:

(a) Polymorphonuclear ('many-shaped nuclei') leukocytes
(polymorphs, granulocytes): formed in the bone marrow,
concerned in the inflammatory reaction, and in the
destruction of bacteria in infections forming pus cells. The
polymorphs are subdivided into neutrophils, basophils
and eosinophils by the staining properties of their granules
with dyes.
(b) Lymphocytes: formed in marrow, passing to lymph
glands, and are of two main groups: B-lymphocytes,
producing immune globulins (antibodies) and T-lympho-
cytes, dependent on the thymus and concerned with tissue
or cellular immunity.
(c) Monocytes: fewer in number but, like the polymorphs,
phagocytic in function (engulfing foreign matter).
The total white cell count (WBC) is 4.0-9.0 x 109/1
(4000-9000/mm 3).
THE BLOOD AND L YMPHA TIC SYSTEM 243
Platelets (thrombocytes) are produced in the bone marrow and
are concerned in blood clotting.
Plasma contains water and electrolytes (e.g. sodium,

potassium, chloride and bicarbonate) concerned in normal
tonicity and acid-base balance and the plasma proteins,
albumin, globulins, fibrinogen and prothrombin. Albumin
(formed in the liver) helps to maintain the osmotic pressure,
keeping fluid in the circulation. The globulins include the
immune globulins, some of which are antibodies. Fibrinogen
and prothrombin are concerned in blood clotting by the
formation of fibrin. Blood also contains a 'fibrinolytic'
mechanism to prevent excessive deposition of fibrin.
Investigations in blood disease

Minimum investigations are haemoglobin, white cell count,
and erythrocyte sedimentation rate (ESR).
It is usually necessary also to stain and microscopically
examine a blood film.
The plasma proteins are measured chemically, and by a
method called electrophoresis, on a paper strip, or immuno-
logically.
Serum iron or ferritin, vitamin B12 and folic acid levels in the
blood may also be measured.
Sternal marrow puncture, using a special hollow needle (local
anaesthesia) and biopsy of enlarged glands may be indicated.
(1) ANAEMIA
Anaemia is a reduction in the number of red cells, or their
haemoglobin content, or both.
General symptoms and signs of anaemia

Any system may be affected.
Cardiorespiratory symptoms are breathlessness, ankle oedema
and sometimes angina.
In the nervous system, effects include tiredness and faint

feelings. Peripheral neuritis, leg pains and loss of reflexes may
complicate any form of anaemia (but are commonest in
pernicious anaemia).
In the gastrointestinal system, symptoms include loss of
appetite, constipation or sometimes diarrhoea.
The characteristic sign is pallor - this may be noted classically
in the conjunctivae, but pallor of the fingers and hands may
also be seen.
ANAEMIA DUE TO BLOOD LOSS

The blood loss may be acute or chronic. (Chronic blood loss is
the most important cause of 'iron-deficiency anaemia'.)
Acute blood loss may be obvious in injuries and gastro-
intestinal bleeding such as haematemesis, but less obvious with
closed fractures or intra-abdominal conditions such as
ruptured spleen, or retroperitoneal haemorrhage complicating
anticoagulant treatment.
Symptoms and signs

Pallor.
Clammy skin.
Apprehension.
Fast pulse and low blood pressure - the picture of haemorr-
hagic shock, requiring transfusion.
The body compensates for such haemorrhage by haemo-
dilution causing a temporary anaemia until the red cells have
been replaced by the activity of the bone marrow, given
sufficient iron.
Chronic blood loss and iron deficiency anaemia

The normal dietary iron content is 10-15 mg daily, meat and
vegetable foods being rich sources. Though only a proportion
of this food iron can be absorbed, it is more than enough to
compensate for the daily iron losses in men, about 1-2 mg.
Thus, men rarely get 'iron deficiency' anaemia from dietary
inadequacy. In women, due to menstrual blood loss, the need
for iron is greater and the demand is increased by pregnancy
and childbirth. The diets of many women do not meet these
needs and 'iron deficiency' anaemia will ensue.
Causes of iron deficiency anaemia

(i) Blood loss: heavy menstrual bleeding (menorrhagia);
chronic aspirin ingestion (causes gastric erosions); peptic
ulcer; carcinoma, especially of rectum, colon or stomach;
bleeds from the nose (epistaxis), and from haemorrhoids.
(ii) Increased demand - fetal needs during pregnancy.
(iii) Dietary inadequacy - occurs in women, and common in
the underdeveloped world.
(iv) Defective absorption - coeliac disease; following
gastrectomy or stomach operation.
Blood examination shows a low haemoglobin and some
decrease in the red cell count; the cells are pale (hypochromic)
and small (microcytic) - iron deficiency gives the picture
described as a hypochromic, microcytic anaemia.
ANAEMIA DUE TO DECREASED BLOOD FORMATION

(a) Lack of building factors such as iron, vitamin B12 and folic
acid. This may occur from:
(i) inadequate dietary intake: iron deficiency is common,
dietary B12 lack very rare, folic acid lack is rare but
may occur in the elderly on a diet poor in 'greens';
(ii) failure of absorption: pernicious anaemia;
(iii) increased demands: anaemia of pregnancy;
(iv) effect of anticonvulsant drugs.
(b) Lack of bone marrow - from infiltration (leukaemia), or
destruction (aplastic anaemia).
(c) Disordered function of the bone marrow.
Pernicious anaemia
Cause
Pernicious anaemia has a familial tendency and is thought to
be a disturbance of immunity arising in adult life. There is an

autoimmune destruction of the parietal cells of the stomach,
and antibodies are detectable in the circulation. The parietal
cells produce hydrochloric acid and also intrinsic factor. Their
destruction is followed by atrophy of the gastric mucosa, and
lack of intrinsic factor. Intrinsic factor is essential for the
absorption of vitamin Bi2 in the lower ileum. In pernicious
anaemia, intrinsic factor is lacking and vitamin B12 cannot be
absorbed.
Vitamin B12 is essential for normal bone marrow function, and
in its absence red cell development is defective.
Symptoms and signs

Occurs in the middle-aged and elderly, and is commoner in
women.
Onset is slow over years.
Pallor.
Low haemoglobin and often mild fever.
The skin has a lemon-yellow tint from the mild jaundice
associated with haemolysis.
The tongue is smooth and often red and sore.
There is anorexia, constipation or diarrhoea.
The spleen may be palpable.
Peripheral neuritis presents as leg pains and loss of sensation,
motor weakness and absent tendon reflexes (lower motor
neurone lesion).
Investigations
The diagnosis is confirmed by:
(1) low haemoglobin, and the typical macrocytic blood film;
(2) megaloblastic marrow on sternal puncture;
(3) low serum vitamin B12;
(4) Achlorhydria: the gastric contents (obtained by tube) are
found to contain no hydrochloric acid, and none is
secreted after an injection of histamine.
Folic acid deficiency
Folic acid deficiency can occur from dietary lack in the elderly
(from inadequate fresh vegetables) and from increased
demands in pregnancy, but is usually due to malabsorption
from the small intestine in tropical sprue and adult coeliac
disease, gut infiltrations and following operations.
The clinical picture is similar to that in pernicious anaemia,
with megaloblastic bone marrow and macrocytic peripheral
blood film, but normal gastric hydrochloric acid. The serum
folic acid level is low.
Anaemia from bone marrow infiltration or destruction

Anaemia in leukaemia, or in marrow infiltration by cancer
metastases (such as from the breast or prostate) is due to the
red cell production being replaced by abnormal proliferating
cells.
Marrow destruction can be caused by X-rays (or nuclear
emissions), poisons such as benzene and lead, and drugs
including gold, and chloramphenicol. These may first depress
platelet production (causing thrombocytopenia), or white cells
(causing agranulocytosis) only later affecting red cell
production, destruction of which causes aplastic anaemia.
Bone marrow function may be depressed in chronic
infections and toxaemia, carcinoma and in renal failure.
INCREASED BLOOD DESTRUCTION - HAEMOL YTIC

ANAEMIAS
Haemolytic anaemia may be due to defects in the red cells, or
to circulating factors in the plasma which cause their
destruction, or to the effects of drugs.
Faults in the red cells

Inherited
(a) Hereditary spherocytosis (congenital haemolytic anaemia,
acholuric jaundice). The red cells are wrongly shaped,
assuming a spherical form instead of their biconcave disc
appearance. These spherocytes are fragile and haemolyse

easily. The spleen is enlarged. The condition occurs mainly
in children, but is rare.
(b) The haemoglobinopathies, where the haemoglobin
molecule is defective.
Sickle cell disease occurs in Negro races and is common
in tropical Africa and the West Indies. In affected persons,
states of anoxia (from high altitudes or following
infections) disturb the abnormal haemoglobin molecule
causing change in shape of the red cells. They become
sickle-shaped, fragile and haemolyse easily causing
episodes of haemolytic anaemia.
Thalassaemia (Cooley's anaemia) occurs in Mediter-
ranean countries and is due to a fetal type of haemoglobin
persisting into adult life, the affected red cells having a
'target' appearance.
(c) Enzyme deficiencies, which increase the susceptibility of
the red cells to haemolysis by substances ranging from
broad beans to many drugs.
Acquired
An example is malaria, where the red cell is invaded by the
Plasmodium parasite, causing its subsequent rupture.
Faults in the plasma

In some cases of severe pneumonia, and in carcinoma,
leukaemia and renal failure, there may be circulating toxins or
'haemolysins' which destroy the red cells.
In autoimmune diseases such as systemic lupus
erythematosus and rheumatoid arthritis these haemolysins
may be identifiable as antibodies - immune globulins.
In certain vascular diseases and nephritis, excessive depos-
ition of fibrin in small vessels may trap the red cells leading to
their fragmentation (microangiopathic haemolytic anaemia).
Transfusing cells of the wrong group, by incompatible
blood transfusion, causes the agglutinins in the plasma of the
recipient to clump followed by haemolysis of the transfused
cells, causing a severe reaction.
The Rhesus factor causes antibodies in a previously
THE BLOOD AND LYMPHATIC SYSTEM 249
sensitized mother; reaching the baby's circulation they will
cause haemolysis of the fetal red cells if the baby is Rh-
positive.
Effects of drugs
Many drugs are capable of causing haemolytic anaemia,
especially in persons whose cells are predisposed from enzyme
deficiencies, or who are already suffering from autoimmune
diseases. Antimalarials and sulphonamides are common
causes but chloramphenicol, nitrofurantoin, phenacetin and
methyldopa may be responsible.
Symptoms and signs of haemolytic anaemia

Jaundice.
Not as deep as in obstructive jaundice.
The urine contains an excess of urobilinogen.
The spleen is enlarged and often palpable.
In severe haemolytic reactions (as may occur with incompat-
ible blood transfusions) there are rigors, fever, prostration and
often severe backache.
In very severe cases, haemoglobin is released into the blood-
stream and appears, with breakdown products, in the urine,
causing acute renal failure.
There is danger of 'sludging' of cells in the kidneys, causing
acute renal failure.
In sickle cell disease, such sludging occurs in peripheral vessels
causing pain and leg ulceration.
(2) THE HAEMORRHAGIC DISEASES

Platelet functions
The platelets can be regarded as plugging up potential holes
which tend to occur in the capillary walls through wear and
tear. Lack of platelets or deficiency of their 'stickiness' results
in purpura and spontaneous bleeding. When a blood vessel
wall is injured platelets collect at the site and liberate

substances which aid vasoconstriction, thus minimizing the
haemorrhage until clotting occurs.
The clotting (coagulation) mechanism has two stages:
(a) The conversion of prothrombin in the plasma to thrombin.
(b) The action of thrombin on the soluble protein fibrinogen
converting it to strands of fibrin, which forms a
meshwork, trapping RBCs and platelets in a clot which
becomes firm by retraction.
Though platelets and calcium are involved in the first stage,
only small quantities are required - even in severe deficiency of
platelets, blood clotting can proceed. The many other factors
needed initially include prothrombin, factor VII and anti-
haemophilic globulin (factor VIII). Deficiency of any of these
factors results in a clotting defect, with a prolonged 'clotting
time' (normally 3-5 min).
In the second stage a deficiency of fibrinogen could prevent
clotting.
Excessive deposition of fibrin in small vessels may occur in
certain vascular diseases, nephritis and malignant hyper-
tension, causing microangiopathic haemolytic anaemia.
Some of the clotting factors may be increased by the
oestrogen component of the combined oestrogen-progestogen
contraceptive 'pill', causing a raised incidence of venous and
cerebral thrombosis in those using such tablets.
The fibrinolytic system

The clotting mechanism is balanced by the fibrinolytic
mechanism which prevents intravascular thrombosis and
breaks down clots that do form, by digesting fibrin.
Over-activity of the fibrinolytic system again results in the
defibrination syndrome and bleeding.
Platelet aggregation is increased by cigarette smoking and
by some of the prostaglandins, but inhibited by aspirin,
dipyridamole and prostacyclin (generated in arterial walls).
Symptoms and signs

Spontaneous haemorrhages into the skin, mucous membranes
THE BLOOD AND LYMPHA TIC SYSTEM 251
and internal organs. The reddish purple spots in the skin (and
mouth) are called purpura, and the spots do not fade on
pressure. Small purpuric spots are called petechiae, and large
confluent areas are called ecchymoses which are bruise-like
discolorations, occurring spontaneously.
There may be bleeding from the nose (epistaxis), mouth and
alimentary tract.
There may be haematuria from renal involvement.
(Senile purpura, seen at the wrists and hands in the elderly, is
due to loss of elasticity of the tissues and slight oozing of blood
from shearing stresses; it is not of serious significance, and not
due to capillary or platelet deficiency.)
HAEMORRHAGE DUE TO CAPILLARY DEFECT

Causes
(i) Infections: severe pneumonia, meningitis (meningo-
coccal septicaemia), subacute bacterial endocarditis (may
be embolic), haemorrhagic chickenpox and smallpox -
toxaemia may be operative in these conditions.
(ii) Vitamin C (ascorbic acid) deficiency - scurvy. Occurs in
elderly from lack of fruit, fresh greens or potatoes, causing
blotchy haemorrhages especially on legs and thickening
of the skin around the hair follicles, bleeding from the
gums.
(iii) Allergic disorders - severe urticaria. Henoch-Schonlein
(anaphylactoid) purpura occurs especially in children;
intestinal bleeding may cause pain, melaena and
precipitate intussusception (herniation of one segment of
intestine into another); there are pains and swelling ofthe
joints. Acute nephritis and renal failure may occur.
(iv) Drug sensitivity - penicillin, sulphonamides, carbromal
(a hypnotic) - causing a haemorrhagic or urticarial rash.
HAEMORRHAGE DUE TO LACK OF PLA TELETS-

THROMBOCYTOPENIC PURPURA
Causes
(i) Poisons and drugs. The platelets are often the first to be
depressed by a poison or drug affecting the bone marrow

and later causing aplastic anaemia - benzene, heavy
metals and gold, chloramphenicol, phenylbutazone and
sulphonamides. Quinine (present in tonic water) may
cause platelet antibodies to be formed.
(ii) Aplastic anaemia - often a complication of these poisons

and drugs.
(iii) Leukaemia and secondary carcinomatosis of the bones -

the platelets are crowded out of the marrow; severe bleed-
ing is common in acute leukaemia.
(iv) Autoimmune diseases, such as systemic lupus erythe-

matosus.
(v) Idiopathic thrombocytopenic purpura. The marrow is

active, but platelets are not properly released.
Children may be affected, the condition in them often
settling spontaneously. In young women there are
recurrent episodes of purpura, spontaneous 'bruising',
and they may have menorrhagia (heavy periods). In
middle age, symptoms can be more severe with haemorr-
hage from mucous membranes and alimentary tract,
haematuria and anaemia. The nurse may be the first to
notice purpura at the flexure of the elbow after taking the
blood pressure: the tourniquet (Hess) test utilizes a short
period of venous occlusion by the sphygmomanometer
cuff in suspected cases. The spleen may be enlarged, but it
not necessarily palpable.
In thrombocytopenia, purpura is liable to occur
when the platelet count, normal 150-350 x 109/1
(15000-350000/mm 3) falls below 40 x 10911. Symp-
toms are severe when the level drops to 10 x 109/1
or below, and this is commonest where the thrombocyto-
penia is a complication of leukaemia or aplastic anaemia.
At these low levels, haemorrhages may be seen in the
retinae using the ophthalmoscope, and there is danger of
intracranial haemorrhage, causing acute stroke or
sudden death.
THE BLOOD AND LYMPHATIC SYSTEM 253
COAGULA TION DEFECT (HAEMORRHAGE DUE TO
CLOTTING FACTOR DEFICIENCIES)
Causes
Prothrombin (and factor VII) are formed in the liver by
vitamin K, a fat-soluble vitamin contained in eggs and greens,
but dietary deficiency is unknown, and normally some vitamin
K is manufactured by bacteria in the intestine. Prothrombin
deficiency is therefore due to:
(i) Failure of vitamin K absorption - obstructive jaundice,
where there is a lack of bile salts, and, rarely, in
malabsorption syndrome.
(ii) Liver dysfunction - cirrhosis, and in the newborn
(haemorrhagic disease of the newborn).
(iii) Effects of drugs - the anticoagulant drugs phenindione
and warfarin compete with vitamin K in the liver,
blocking the formation of prothrombin - this is the basis
of their therapeutic effect. Large doses of aspirin have a
similar action. The breakdown of these drugs is increased
by barbiturates and if the latter are added and
subsequently withdrawn, rebound bleeding may occur.
Anticoagulant overdosage may present with haem a-
turia, epistaxis or skin haemorrhages, and in all coagula-
tion defects the blood is slow to clot after injury.
Haemophilia
Haemophilia is due to deficiency of factor VIII, anti-
haemophilic globulin. It is a sex-linked genetic disorder; thus it
is transmitted by apparently normal females carrying the trait
in one of their X chromosomes, and it affects only males.
Young boys are affected, but most now reach adult life.
Patients bruise easily, and their blood does not clot well after
injuries or dental extractions - there is a slow persistent ooze.
Haemorrhage may occur into joints, causing pain and severe
deformity if untreated.
Defibrination syndrome
This presents as continued severe bleeding and occurs in
concealed accidental haemorrhage in pregnancy (retro-

placental bleeding), and following operations on the prostate
or lungs. In both these situations there has been much bleeding
and its continuation is due either to massive intravascular
coagulation using up all the body's fibrinogen, or to excessive
action of the fibrinolytic system attempting to dissolve the
clots.
The diagnosis is established by finding a lack of fibrinogen
in the blood, and there is failure of clot retraction when blood
is allowed to clot in a test tube.
(3) POLYCYTHAEMIA
In polycythaemia there is an excess of circulating red cells,
perhaps 7-8 x 1012/1 instead of the usual 5 x 1012 /1 (7-8
million instead of 5 million/mm3), a raised haematocrit
(packed cell volume; normal 450/0) and raised haemoglobin
(over 120%).
Polycythaemia may be secondary to the anoxia of living at
high altitudes, chronic lung disease (such as chronic bronchitis
and emphysema) or cyanotic congenital heart disease.
Symptoms and signs

A feeling of fullness in the head, giddiness and fatigue.
'Ruddy' cyanosis.
A tendency to venous and arterial thrombosis and strokes.
A bleeding tendency.
Pruritus.
The spleen is enlarged in two-thirds of the cases.
(4) THE LEUKAEMIAS

Leukaemia is a neoplastic, malignant process affecting the
white cells of the blood. Either the polymorph (the myeloid
series), lymphocyte or monocyte series may be involved. There
is an abnormal, progressive accumulation (hyperplasia) of
cells in the haemopoietic tissues (bone marrow, lymph glands,
spleen and liver) throughout the body and in chronic
leukaemias increased circulating white blood cells.
Causes
In acute leukaemia the white cells fail to differentiate properly
and build up in the bone marrow or lymph glands. In chronic
leukaemia the accumulation may be due to a disturbance ofthe
mechanism regulating the number that is normally produced.
The cause or causes are often obscure, but there is an increased
incidence of leukaemia after exposure to X-rays or thermo-
nuclear emissions as in the survivors of the atomic bomb
explosions at Hiroshima and Nagasaki in 1945. A virus cause,
an enzyme defect or a disorder of immunity are other possible
causes.
Acute leukaemia
Acute leukaemia occurs especially in children and the cause is
unknown. There is an accumulation of early cells ('blast' cells)
in the marrow and lymph nodes. These cells fail to different-
iate properly into their appropriate series, and crowd out other
white cells, red cells and the platelets. The most common type
in children is acute lymphatic (lymphoblastic) leukaemia, but
in adults acute myelogenous leukaemia is equally common.
Symptoms and signs

A rapidly developing anaemia.
Haemorrhages (from platelet lack) from the gums and into the
skin, bones and joints (causing severe pain in the latter) and
internal organs, including the brain.
Fever, and susceptibility to infections.
Enlargement of lymph glands and spleen.
(Investigations include blood film and bone marrow examin-
ation.)
Chronic myeloid (granulocytic) leukaemia

The bone marrow and lymph glands are taken over by
abnormal cells usually found to contain an abnormal chromo-

some. There is a progressive accumulation of granulocytes
(polymorphs) with an excess in the peripheral blood.
Symptoms and signs

Commonest in young adults.
Gradually increasing tiredness and weakness due to anaemia.
Enlargement of lymph glands, liver and spleen causing
discomfort and 'dragging' sensation in the abdomen. Purpura
and haemorrhages may occur.
Deposits in the skin and pruritus.
A raised metabolism with weight loss, sweats and raised blood
uric acid causing gouty symptoms such as joint pains.
(The diagnosis is confirmed by finding a raised white blood cell
count, sometimes over 100 x 109/1 (normal 4-9 x 109/1) in
the peripheral blood, and by sternal or iliac marrow puncture.)
Chronic lymphatic leukaemia

The bone marrow is gradually infiltrated and eventually
replaced by an accumulation of lymphocytes, also present in
lymph nodes, spleen, liver and in the peripheral blood. In
addition to progressive anaemia, the immunity function
becomes defective and patients are prone to infection.
Symptoms and signs

Commonest in middle-aged and elderly men.
Tiredness, weakness.
Gland swellings and enlargement of the spleen.
May be remarkably benign in the elderly, being discovered
sometimes at a blood count during investigations of
pneumonia or other infection, or incidentally at a hospital
attendance for another reason.
(The diagnosis is confirmed by a total white cell count of up to
tOO X 10911 (lOO OOO/mm3), 90070 of the cells being lympho-
cytes.)
Agranulocytosis
An absence or greatly decreased number (leukopenia) of white

blood cells of the 'granular' series, the polymorphs, in the
peripheral blood.
The cause is bone marrow depression, and the factors
responsible are the same as in aplastic anaemia and thrombo-
cytopenia, though some substances are more selective in
destroying the white cells than the red cells or platelets.
The following drugs are the important causes:
phenylbutazone (butazolidin),
chloramphenicol,
anti-thyroid drugs such as carbimazole and methyl-
thiouracil,
the cytotoxic drugs.
Symptoms and signs

The patient is prone to infection, and the first symptom is
often a sore throat.
Marrow depression occurs over a longer period.
Fever and toxicity.
(5) DISORDERS OF THE SPLEEN AND LYMPH NODES

The spleen and lymph glands are the important filters in the
defence system against foreign matter or organisms. The
spleen is the filter for the circulating blood. The lymph glands
are the filter for organisms arriving from the mucous
membranes and skin via the lymphatics.
Functions
(a) Blood formation - the spleen's haemopoietic function can

be increased if there is undue demand, or in marrow
failure. The spleen has little reservoir function for red cells
in man, but may store platelets.
(b) Blood destruction - the reticulo-endothelial cells remove
red cells from circulation at the end of their 120-day life
span.
(c) Defence against infection and participation in the immune

response.
Causes of enlargement (splenomegaly)

(a) Infection - any severe, acute infection especially if there is
bacterial invasion of the bloodstream as in typhoid fever or
septicaemia ('septic' spleen):
subacute bacterial endocarditis;
chronic infections, especially tropical parasitic infec-
tions such as malaria and kala-azar (trypanosomiasis).
(b) Blood diseases:
polycythaemia, myelosclerosis;
the leukaemias;
haemolytic anaemia, idiopathic thrombocytopenic
purpura.
(c) Diseases of lymphoid tissue - Hodgkin's disease.
(d) Cirrhosis of the liver - causes portal venous obstruction.
Effects of splenomegaly
The spleen has to enlarge to about three times normal size
before it becomes palpable. Enlargement is greatest in the
tropical diseases, myelosclerosis and chronic myeloid
leukaemia, where the size of the organ may cause discomfort.
The spleen has an influence on bone marrow function,
possibly hormonal, and 'hypersplenism' prevents release of
cells from the marrow, causing anaemia, leukopenia or
thrombocytopenia.
THE LYMPHATIC SYSTEM

Lymph is tissue fluid that enters the tiny lymphatic capillaries
which join to drain it into the regional lymph nodes, where
lymphocytes are added. The larger lymphatics terminate
mainly in the thoracic duct, which enters the left subclavian
vein at the root of the neck thus reaching the great veins near
the heart. The lymphatic drainage of the small intestine is also
an important route of fat absorption.
The lymphoid follicles in the lymph nodes produce the
lymphocytes concerned in humoral antibody and plasma cell
formation.
Causes of lymph gland enlargement

(a) Infections: local, as from a septic fauces or sore throat:
tuberculosis (and sarcoidosis) generalized, as in glandular
fever (infectious mononucleosis).
(b) Metastatic: from spread of tumour cells along the
lymphatics (for example axillary gland involvement from
carcinoma of the breast).
(C) Primary malignant conditions of the haemopoietic system
such as leukaemia, or of the lymphoreticular system - the
reticuloses, such as Hodgkin's disease.
THE RETICULOSES
The cause or causes of the malignant reticuloses is unknown,
but interest has been aroused by the finding of a rather similar
tumour affecting the jaw and pharynx of children in tropical
East Africa. This tumour was described by Burkitt and is
called Burkitt's lymphoma. In some cases the cells contain a
virus which may be transmitted by mosquitoes, and a similar
virus may be found in glandular fever.
(a) Hodgkin's disease (lymphadenoma, malignant

lymphoma)
Symptoms and signs
Commonest in young adults.
Swellings of the lymph glands, often first in the neck, the
glands being rubbery but not tender.
Glands in the mediastinum (root of the lung) or abdomen may,
however, be involved first, making diagnosis difficult -
lymphatic blockage here may cause chylous ascites, or pressure
on the veins may cause leg oedema.
Generalized glandular enlargement with enlarged spleen and
liver.
Fever, weakness from anaemia.
Loss of weight and pruritus.
DIFFERENTIAL DIAGNOSIS OF ANAEMIA

Onset Pre-existing conditions
Anaemia - due to may be acute pallor, tachycardia, dyspnoea -

blood loss or chronic may be post-traumatic or
surgical; fatigue, angina
Anaemia - due to chronic peptic ulceration, salicylate

iron deficiency usage, carcinoma, pregnancy,
malnutrition; commonest in
women
Anaemia - due to chronic, may hereditary, haemoglobin or RBC

haemolysis be acute if abnormality; malaria drug
induced usage, incompatible blood
transfusion; chronic symptoms
of anaemia
Pernicious anaemia chronic, middle-aged, elderly and

over years predominantly female;
anorexia, constipation,
fatigue and chronic
symptoms of anaemia
hypotension if acute, shock; routine RBC may not be abnormal

melaena, menorrhagia in sudden loss, chronic loss gives
reticulocytosis, low serum iron, Hb
menorrhagia, coeliac disease low Hb, decreased RBCs, hypo-

chromia, microcytosis, faecal occult
blood positive; may have low serum
folic acid as well as iron
Negroid or Mediterranean low Hb, haemoglobin electrophoresis,

racial origin; jaundiced, may have porphyria, or sickle cell;
spleno/hepatomegaly G6PD deficiency; may have
positive Coombs' test
glossitis, splenomegaly; low Hb, macrocytic film;

peripheral neuritis megaloblastic sternal marrow;
low serum B12
Investigations
Apart from anaemia and raised ESR, there are no specific
findings in the peripheral blood. There may be infiltration of
the bone marrow but the diagnosis of Hodgkin's disease is best
confirmed by gland biopsy; lymphangiography defines its
extent.
(b) Lymphosarcoma and reticulum cell sarcoma

These are malignant tumours of lymphoid tissue, involving
lymphocytes and reticulum cells respectively. One of these cell
types displaces all the others in lymph nodes, spleen, bone
marrow or thymus gland. The process is much more rapid than
in Hodgkin's disease and the cells spread into neighbouring
tissues as well as spilling out via the lymphatics and blood-
stream causing widespread dissemination of the growths. The
condition may terminate as acute leukaemia.
Symptoms and signs

Similar to Hodgkin's disease, one group of nodes being first
involved or the process presenting in several areas.
Mediastinal and retroperitoneal lymph nodes are frequently
involved, causing discomfort, pressure symptoms and
recurrent pleural or peritoneal effusions.
Lesions may start in the tonsils, stomach or other part of the
alimentary tract, or present in the skin.
Malaise, fever, sweating and weight loss.
Anaemia occurs, sometimes haemolytic in type.
The diagnosis is confirmed by biopsy, which shows sheets of
neoplastic cells of one cell type, different from the mixed cells
in Hodgkin's disease tissue.
(c) Myelomatosis (multiple myeloma)

This condition occurs in the middle-aged and elderly, is
commoner in men and is a malignant process usually arising in
the bone marrow. Thus the marrow of flat bones such as the
vertebrae and skull becomes infiltrated with plasma cells,
called myeloma cells. There are single or multiple osteolytic
(bone-destructive) lesions in the bony skeleton. The myeloma
cells produce abnormal immunoglobulins, a product of which
may appear as Bence Jones protein in the urine (see below).
The cause is unknown.
Symptoms and signs

Bone pain and backache.
Fever, weight loss.
Anaemia and sometimes a bleeding tendency from thrombo-
cytopenia.
Patients are prone to infection.
The weakened bones may fracture causing root pains such as a
bilateral 'sciatica' if the vertebrae are involved.
The abnormal proteins may be deposited as amyloid tissue in
nerves or organs including the tongue.
Deposits of protein in the renal tubules may cause renal
failure.
Investigations
The ESR is raised - myelomatosis is a condition often
associated with a very high ESR, 100 mm/h or more; such a
finding may lead to the diagnosis in a patient with few
symptoms. The abnormal proteins can be characterized by the
procedure called paper strip electrophoresis, or by immuno-
logical methods.
On heating the urine, Bence Jones protein is detectable as a
cloud around 70 o e, which disappears on boiling and
reappears on cooling. When present, it is virtually diagnostic
of myelomatosis.
X-rays show rarefaction or punched-out areas in the bones.
Chapter 14
The Psychological System
Psychological disorders, emotional and psychiatric, account

for at least 20070 of all medical consultations. Anxiety and
depression form at least half of these, and the incidence in
females is twice that of males. Hospitalization is (in order of
frequency), for depression and suicide attempts, schizo-
phrenia and other psychotic disorders, personality disorders,
alcoholism, dementia and mental handicap. The most
frequent cause of admission is for drug overdosage - now in
some countries the single most frequent cause of all admissions
to general hospitals. Suicide - self-poisoning - is the main
cause of death in disorders of the psychological system.

(A) disturbances of behaviour,
(B) psychological test performance,
(C) blood and urine tests (in drug abuse or overdosage).

(1) psychological confusion: depression, anxiety, delusion,
hallucination, coma;
265
(2) weight loss/excessive gain;

(3) multiple symptoms with suggestions of a physical hypo-
chondria.
(A) DISTURBANCES OF BEHAVIOUR

Whilst history-taking or pursuing reported complaints of the
psychologically disturbed patient, an irrationality and
disconnected thought pattern can become obvious.
Demeanour or dress, evidence of self-neglect, or inability to sit
quietly describing symptoms soon reveal the disturbed
personality. In doubt, relatives should always be interviewed
as well as the patient.
(B) PSYCHOLOGICAL TESTS

Specific tests of intellectual/intelligence function can only be
efficiently administered by those trained in their interpretation
- simple tests of function with regard to asking name, date and
for topical current information reveal inadequacies or
confusional states.
(C) BLOOD AND URINE TESTS
In the overdosed or comatose patient, serum or urine levels for

the commonly used or available drugs are essential for
diagnosis and therapy management. It should always be
recalled, however, that the suicidal patient may nevertheless
have intercurrent physical disease and full health status assess-
ment should be undertaken.
Common Disorders of the Psychological

System
(1) MENTAL SUBNORMALITY (MENTAL
RETARDATION)
Failure of normal brain development.
THE PSYCHOLOGICAL SYSTEM 267
Causes include
chromosome abnormality, e.g. mongolism (Down's
syndrome);
gene abnormality - phenylketonuria, an enzyme defect,
excess amino acid (phenylalanine) damages brain;
damage to embryo - rubella (German measles) and toxo-
plasmosis in early pregnancy;
injury at birth;
post-natal- infections (e.g. meningitis); hypothyroidism if
untreated (cretinism).
In many cases the cause is unknown.
The mentally subnormal may be assessed educationally
according to Intelligence Quotient (IQ). Normal IQ is taken as
100. Those with an IQ over 80 may be educable normally, IQ
50-80 are subnormal and require special schooling, IQ under
50 are severely subnormal. Personality and emotional adjust-
ment, family and social background influence management.
The mentally handicapped may be better accepted in a rural
community than in an industrial city.
(2) MENTAL ILLNESS

There are three main types of mental illness:
(a) due to an organic lesion;
(b) non-organic - psychiatric;
(c) personality disorders.
(a) DUE TO AN ORGANIC LESION

Where a known physical disease affects the brain, e.g. neuro-
syphilis, cerebral tumour, or arteriosclerosis, dementia, deter-
ioration of intellect and memory, may result.
Toxic confusional states (delirium)

A toxic confusional state of delirium results from disordered
function of the brain:
Causes
An organic cause - fever, infection, toxaemia, electrolyte
depletion, hepatic failure (portal systemic encephalopathy),
poisoning with alcohol or drugs, and, any condition causing
cerebral anoxia;
A slight decrease in the oxygen supply to the brain cells is
especially important where there is pre-existing brain damage
or degeneration (as in dementia);
Thus respiratory infection or heart failure are common causes
in the elderly - a toxic confusional state is reversible if the
cause can be treated.
Symptoms and signs

There is clouding of consciousness;
Disorientation, confusion;
Restlessness;
Often accompanied by hallucinations (false perceptions);
The differentiation from an acute behaviour disturbance
accompanying psychiatric illness such as schizophrenia or
hysteria is not usually difficult, for in these there is no back-
ground of physical illness.
Dementia
Dementia is a deterioration of mental function following brain
damage or disease - such damage is usually severe and
extensive.
Causes
Dementia is usually a result of slowly progressive cerebral
disease and is commonest in old age.
Senile dementia is seen especially in women and may be an
ageing change - the brain undergoes shrinkage and plaques of
degenerate tissue may be found at autopsy. Arteriosclerotic
dementia also occurs in the elderly, especially in men, but can
usually be differentiated by its association with previous
strokes or other evidence of cerebral arterial disease, with or
without hypertension: the deterioration of personality may
not be so complete.
The pre-senile dementias are a group of conditions presenting
in patients below the age of 60, e.g. Alzheimer's disease
(probably an early form of senile dementia), Pick's disease,
Huntington's chorea, and others - all relatively rare.
Neurosyphilis (OPI).
Cerebral tumour.
Chronic alcoholism.
Deficiency of thyroxine in myxoedema, or of vitamin B12 in
pernicious anaemia are unusual causes.
Acute injury is a rare cause, but the repeated brain trauma
sustained by boxers may lead to dementia.
Symptoms and signs

Impairment of intellect, associated with impairment of
memory - the patient has a loss of memory for recent events
but may be able to recall happenings of many years ago.
The memory disturbance causes disorientation in time and
place.
A deterioration and coarsening of personality, and emotions
may be shallow or disturbed.
Social behaviour disintegrates, personal appearance and
hygiene are neglected.
The patient may become filthy in his toilet habits.
Conversation with the patient, enquiries as to name, address,
age, and family ties, day of the month, current events, simple
arithmetic (subtracting 7 from 1(0), giving numbers to
remember - these usually suffice to confirm the diagnosis.
Dementia is usually a permanent state, but symptoms may be
worsened by intercurrent infection or anoxia, especially in the
elderly.
(b) NON·ORGANIC
(1) Anxiety and depressive states - a disturbance of the
emotions or 'affect'. The patient retains his insight - he
realizes he is suffering from such a state. Anxiety neuroses

include obsessive-compulsive states and phobias (irra-
tional fears). Depressive illness is extremely common in
all societies.
(2) Psychosis - a severe disorder in which the patient fails to
realize he is mentally ill. Schizophrenia is the classical
example, and the patient may be completely detached from
reality.
(3) Psychosomatic and hysterical disorders - the patient has
symptoms for which there is no physical basis.
Anxiety and depressive states

Anxiety and depression are extremely common. They may not
be complained of, but will be admitted to, in many patients
attending hospitals ostensibly with other complaints. They
may be regarded as exaggerations of normal response to a
stressful situation, grief and bereavement. While they may
exist in 'pure' form as anxiety state and depressive state, they
are commonly inseparable.
Symptoms and signs
A severe depressive state may present as anxiety.
Fears and feelings of unworthiness and guilt.
Complaints of sleeplessness and of feeling 'always tired'.
Depression may be classified as 'reactive' (i.e. reaction to an
existing stressful situation such as financial trouble or a broken
love affair), or 'endogenous' (in which the personality may
basically be a depressive one and there may be a family
history).
The reactive depressives have difficulty in getting off to sleep,
whilst the endogenous depressives wake up in the small hours
feeling extremely low in spirits and unable to get back to sleep.
Severe cases become extremely miserable and withdrawn, and
unable to pursue their normal activities.
Concentration at book work becomes impossible.
Such patients may attempt suicide as the only relief from their
misery.
The psychoses
A psychosis or psychotic state is a severe mental illness, in
which the patient has no insight, and is often detached from
reality.
The cause is unknown, but there may be a genetic predis-
position and a biochemical abnormality in cerebral amine
metabolism.
Symptoms and signs

Swings of mood from melancholia to acute excitement and
violence amounting to mania. This is manic-depressive
psychosis.
In mania, the patient appears uncontrollably excited with
flights of idea, delusions (false beliefs) and hallucinations
(false perceptions, the patient hearing or seeing things that are
not there).
The term schizophrenia or schizophrenic psychosis is used to
describe mental illness characterized by:
deterioration of emotional stability and personality;
disordered judgement; and
failure to act in accord with reality.
Schizophrenia presents in young people who, having been
apparently normal, become withdrawn, decline to mix with
others, and develop disorders of thought and of emotion.
Abstract thinking is impaired, the thought process may
suddenly become 'blocked' and the patient may believe that
his thoughts are being influenced by outside sources - he may
hear voices (auditory hallucinations), and there may be
delusions of persecution, the paranoid state.
There is emotional flattening with swings from apathy to
inappropriate laughter or outbursts of rage with aggression
and destructiveness.
Mild cases often go unrecognized, the patient presenting

himself repeatedly at hospital with many complaints, for
which multiple investigations may have been carried out. The
clue to such a state is the difficulty the doctor experiences in
attempting to get a lucid history - after an hour's interview, he

feels no further forward in the consultation.
(e) PERSONALITY DISORDERS
(1) Psychopathic disorder. A psychopath is a person who fails

to conform to accepted social standards or conduct
without being aware that he may be doing wrong. Psycho-
paths may be aggressive, creative, or socially inadequate.
(2) Alcoholism and drug dependence. Dependence exists
when a person is compelled to take a drug for its psychic
effects. Withdrawal may result in feelings so unpleasant
that the habit is resumed.
It is becoming clear that many so-called mental disorders have
a physical cause. Thus depression may be due to disturbed
function of the emotional system connected with the hypo-
thalamus, some schizophrenics have an abnormality of amine
production, and an extra Y chromosome may be found in
some criminal psychopaths. These considerations apart,
physical illness may present as a mental illness such as
depression. Again, the mental state of the patient affects his
reaction to systemic disease.
Thus the division of mentally ill patients into a group to be
kept apart in a special institution is no longer justified. The
disturbed behaviour associated with mental disorders was
often due to lack of understanding by relatives or doctors,
leading to resentment and agitation in the patients who were
quite unjustifiably confined behind locked doors. Some of the
symptoms attributed to mental illness were in fact due to such
institutionalization and social isolation. Modern psychiatric
units are therefore part of the general hospital service.
Psychosomatic and hysterical disorders

Where there appears to be no physical basis for complaints,
they are often labelled 'psychosomatic' or 'functional' or
'psychoneurotic' .
In hysteria the symptoms multiply and exhibitionism
increases in front of an appropriate audience.
Hysteria is used in a different sense to describe a mental state
in which part of normal consciousness is missing or 'detached' .
Symptoms and signs
There may be a hysterical paralysis of a limb, or the patient
may fail to appreciate painful stimuli such as pin-prick, the
sensory loss not conforming to a recognized pathological
pattern.
Severe complaints may be described by a patient whose smiling
appearance is incompatible with them.
Occasionally there may be memory loss or a 'fugue' in which
the patient apparently does not know his or her identity and
may be found wandering, by the police.
Hysterical fits, not of the pattern of true epilepsy, also occur.
The cause of such hysterical symptoms is uncertain, but
personal gain may be the motive, albeit at subconscious level.
Anorexia nervosa
This is a condition found in the young. They stop eating, with
marked loss of body weight, presenting an extreme emaciation
in severe cases. The cause may be related to emotional disturb-
ance or to an obsession that they are too fat and they proceed
to put themselves on a starvation diet. They then develop a
curious lack of insight into the fact that their physical appear-
ance has become less, instead of more attractive. Amenor-
rhoea is usually present, but the secondary sexual character-
istics such as pubic and axillary hair, are retained. Severe cases
may go on to extreme weakness and death.
ALCOHOLISM
Acute alcoholic intoxication
The effects are well known - disturbance of balance,
dysarthria, emotional and intellectual changes. Alcohol is a
cerebral depressant, and while inhibitions may be released,
judgement is impaired. There is a high association with road
traffic accidents. Alcohol is also a gastric irritant, and a
diuretic.
Chronic alcoholism
The alcoholic, or alcohol-dependent person, is one who has
lost control of his drinking and cannot stop. He should be
distinguished from the regular heavy drinker, who can still
stop if advised to do so - signs of alcoholic poisoning such as
peripheral neuropathy, cirrhosis, or alcoholic heart disease
and failure are good reasons for this advice.
It is estimated that 1070 of the population are alcoholics, but
many conceal their addiction. They do not usually display
signs of acute drunkenness, but their lives revolve around their
need for alcohol. Alcoholism may follow excessive social
drinking in those of previously good personality, or the habit
may have followed a drinking bout after depression or stress,
an escape from the 'cares of the world'. Some alcoholics have
underlying psychotic disorders, many are psychopaths and the
history often includes a broken home and family alcoholism.
Symptoms and signs

Morning drinking or solitary drinking may be the first signs.
The 'shakes' occurs on rising, following the withdrawal of
alcohol during the period of sleep - there is tremor and irrit-
ability, and the subject reaches for another drink.
Gradually there is deterioration of personality and concent-
ration at work, and all money is diverted to procuring alcohol
- cheap wines (and sometimes methylated spirits) replacing the
previous spirits.
Delirium tremens (DTs) is caused by intercurrent infection or
sudden withdrawal of alcohol. Delirium is a state of clouding
of consciousness, with restlessness and hallucinations - here
they frequently take the form of small animals running over
the body.
There is fear, confusion, and a tremor.
Encephalopathy is due to the vitamin B} deficiency common in
the alcoholic, from poor diet.
There are haemorrhages at the base of the brain, causing
confusion, paralysis of eye muscles with visual upset such as
diplopia, nystagmus and ataxia.
This may proceed to loss of memory for recent events, and
confabulation, the patient giving a fictitious account of his
movements.
In the late stages of alcoholism there is progressive degener-
ation of cells in the cortex of the brain, with memory loss,
intellectual deterioration and complete disintegration of
standards of personal hygiene and behaviour.
DRUG DEPENDENCE (ADDICTION)

Dependence may be defined as a compulsion to take a drug on
a continuous or period basis in order to experience its psychic
effects and sometimes to avoid the discomfort of its absence.
Thus withdrawal of some drugs of dependence results in
symptoms such as agitation and anxiety - the brain has
adapted to the drug and its absence may cause such symptoms,
which may be related to a rebound excess activity of dream
(REM) sleep. Tolerance to the drug, that is the need to take
increasing doses to produce an effect, may or may not be
present. Tolerance may be due to the production of increased
enzymes by the liver, speeding destruction of the drug.
The introduction of opiates (morphine and heroin) has been
followed by their misuse and dependence. Heroin mixed with
cocaine (H and C) and injected intravenously ('mainlining')
has euphoriant effects. These are powerful drugs of depend-
ence and tolerance, so that subjects have to procure further
supplies. Tight control has resulted in some improvement in
heroin abuse in Britain, and addicts can only be supplied at
special clinics. In the United States, however, heroin addiction
remains a major problem.
Cannabis (marihuana, hashish, hemp, 'pot') is commonly
smoked or eaten. It is said to remove inhibitions and improve
the mood, giving a feeling of peace, but its effects are partly
dependent on the subject's existing frame of mind and his
social surroundings. Cannabis also causes dilatation of the
conjunctival vessels. The smoke has a characteristic smell.
Although there is no proof that its use has resulted in serious
harm or dependence, those who smoke cannabis are at risk
from their social associations with others who may use more
dangerous drugs.
DIFFERENTIAL DIAGNOSIS OF ANXIETY AND

DEPRESSION
Onset Characteristics (subjective)
Anxiety acute or subjective feeling of apprehension,

chronic unease, tension, terror or panic;
somatic complaints of headache,
dyspnoea, hyperventilation,
palpitation, dizziness, tremor,
restlessness, fatigue, sweating;
late night insomnia, anorexia
Depression usually chronic, pessimism, despair, sadness and

may be acute irritability that is persistent;
(e.g. grief) feelings of guilt, hopelessness,
apathy; may be dramatic or
delusional; may follow a swing
from mania or hyperactivity in
the young, may be more long-
lasting in the elderly; obsessional
and paranoid thoughts; anorexia,
constipation, loss of libido, crying
spells, early morning waking
Characteristics (objective) Laboratory

investigations
affects women more than men, Reassurance: by complete

onset in adolescence or early blood count, urinalysis,
adulthood; episodes of abrupt thyroid function tests, OTT
onset; phobias and depressive (if any evidence of hypo-
reactions; frequent gastrointes- glycaemia); chest X-ray,
tinal disturbance; suicide rare exercise tolerance ECO,
routine GIT investigation
affects elderly more than young, To exclude organic cause:

recurrent episodes become more complete blood count,
chronic; may be agitated, careless urinalysis, serum electro-
of personal hygiene, memory lytes, thyroid function tests,
impairment, delusions common, chest X-ray, ECO, OIT
mental concentration deteriorates; investigation
suicide common
LSD (lysergic acid diethylamide) and other derivatives

produce hallucinations and may cause brain damage.
Almost any sedative or stimulant drug can be misused. Thus
amphetamines cause stimulation but also psychotic episodes.
Apart from such effects, intravenous use and sharing of
syringes may result in sepsis and hepatitis. Amphetamines
have little medical application, and curtailment of prescribing
has resulted in less misuse. Thus drug-takers have turned to
barbiturates and non-barbiturate hypnotics often mixed with
alcohol, in their search for psychic effects.
Recent research suggests that disturbed beta-endorphin
secretion in the brain may be related to drug and alcohol
dependence.
(3) SELF-POISONING - ATTEMPTED SUICIDE

The vast majority of persons who take an overdose of drugs do
so as an impulsive gesture, as a 'cry for help'. They will gener-
ally be admitted to hospital and they realize that their action
affords an opportunity for their misery to be attended to. Only
a small proportion intend to kill themselves and they make a
planned attempt away from the public gaze, and, if foiled, try
again. The term 'self-poisoning' is now therefore preferred to
cover all cases with or without serious suicidal intent. Self-
poisoning accounts for over 1OlrJo of acute admissions to
British hospitals.
Corrosive acids and coal gas used to be the common
methods, but the former is now regarded as unpleasant, and as
natural gas contains no carbon monoxide, attempts with gas
are ineffective. Car engine (petrol, not diesel) exhausts are,
however, a source of carbon monoxide (and inadequate
combustion or ventilation using any fuel can result in its
production).
CARBON MONOXIDE POISONING

The gas fixes to haemoglobin, forming carboxyhaemoglobin
and preventing oxygen carriage by the blood. Although carb-
oxyhaemoglobin is pink, patients suffering from poisoning
appear pink only if moribund. Earlier they are cyanosed and
pale, confused or unconscious; breathing is maintained to a
late stage.
ASPIRIN (SALICYLATE) POISONING

Acute aspirin poisoning does not initially cause unconscious-
ness in adults - even drowsiness is unusual though it does occur
in children. If an adult patient with aspirin poisoning is
unconscious, he is either at death's door, or another drug has
been taken in addition.
Aspirin stimulates the respiratory centre causing rapid deep
breathing. Though normal doses are antipyretic, overdosage
causes metabolic stimulation, restlessness, pyrexia and
sweating. There is tinnitus (noises in the ears). Gastric irrit-
ation causes vomiting and the patient becomes dehydrated. An
initial respiratory alkalosis (due to over-breathing washing out
C02) is followed by metabolic acidosis. There is potassium
upset and hypokalaemia. Aspirin competes with vitamin K,
resulting in lowered prothrombin level and bleeding tendency.
PARACETAMOL (ACETAMINOPHEN) POISONING

Paracetamol is contained in many proprietary analgesics and
self-poisoning with the drug is now common - fatalities have
occurred after ingestion of 10 g. Early symptoms include
nausea, pallor and sweating but these may not be marked.
Coma is not a feature unless other drugs have been ingested as
well. Paracetamol overdosage damages the liver. An early
assessment of the severity of the poisoning by measurement of
blood paracetamol levels (a 4 h level over 200 mg/l being
dangerous) is essential if treatment, which should be started
within 10 h of ingestion, is to be effective.
Chapter 15
The Common Infections*
Almost half of any population at risk will be affected by one or

other of the common infectious diseases in anyone year. In the
developed world, however, largely due to improvements in
nutrition, the environment, and the use of antibiotics for the
treatment of complications, specific infectious diseases -
upper respiratory, chickenpox, measles, mumps, TB and
hepatitis - account for less than 1070 of deaths and less than 2%
of hospital admissions.

(A) blood tests, routine and for antibodies;
(B) exudates and mucus secretions for bacterial/viral identi-
fication;
(C) chest X-ray, where necessary.
Common symptoms of disorder will be:

(1) fever;
(2) anorexia, fatigue, malaise;
* See also chapter 5.
281
(3) rash;
(4) pain - headache, muscular, arthralgia or localized;
(5) nasal, skin, mucus discharge.
(A) BLOOD TESTS

The presence of specific disease detected by antibody form-
ation depends on the time taken by the infected person to
develop that response. Blood test initially demonstrating white
cell changes brought about by a viraemia therefore may need
to be repeated after a time interval to identify the specific
antibody - rubella, infectious mononucleosis, influenza,
brucellosis etc. - especially by means of a rising titre. Blood
tests to identify the presence of the malaria parasite may only
prove positive if taken at the time of the high fever. Diagnosis,
therefore, by blood test is often only confirmatory of the
suspicion engendered by the clinical signs.
(B) EXUDATE CULTURE

Viral growth from swabs of nasal discharge is not always
readily available. Tubercle bacilli identification may require
culture in living animal tissue and take time to achieve;
gonococcal identification may be simply achieved by the
immediate examination of a stained slide of urethral
discharge. Thus a variation in the requirements of the labor-
atory for the identification of the specific disease may mean
again that the diagnosis is confirmed, and not initially made by
the bacteriology involved.
(C) CHEST X-RAY
This can be specific in cases of respiratory tuberculosis.
Common Infectious Diseases

(1) MEASLES
Measles is a virus infection usually affecting the young.
THE COMMON INFECTIONS 283
Symptoms and signs
Malaise, headache, fever.
Nasal discharge.
A rash involving the face and neck, spreading over the body.
White spots in the mouth near the molar teeth, Koplik's spots,
may appear earlier, and are diagnostic.
Secondary bacterial invasion may cause middle-ear infections
and pneumonia - while such complications are rare in the
healthy, they are a common cause of death in measles
outbreaks in underdeveloped countries.
(2) GERMAN MEASLES (RUBELLA)

Rubella is a virus infection.
Symptoms and signs
Mild malaise.
A pink rash about the neck, face, chest and abdomen.
Lymph gland swellings, especially the glands at the back of the
neck. (The virus infects the developing embryo in the
pregnant, resulting in congenital defects in the heart, brain,
eye and ear.)
(3) SCARLET FEVER

Symptoms and signs
A scarlet rash, mainly affecting the trunk, occurring at the
height of a haemolytic streptococcal sore throat.
The organism produces a toxin which affects the skin.
(4) WHOOPING COUGH

Symptoms and signs
The upper respiratory passages are affected, with appearances
of a cough and cold.
The cough is followed by an inspiratory 'whoop' from laryn-

geal narrowing.
There may be vomiting.
(5) DIPHTHERIA
A bacterial infection of the throat causing pain.
Symptoms and signs

A 'dirty grey' membrane at the tonsillar region.
Cervical lymphadenopathy .
The production of a toxin affecting the heart and nervous
system.
Any suspicion of this infection indicates the need for a throat
swab to confirm diagnosis. Diphtheria may occur as an infec-
tion of the larynx alone and should be borne in mind in cases of
hoarseness with systemic upset.
(6) CHICKENPOX (VARICELLA)

The virus is the same as that causing herpes zoster (shingles) in
adults. Susceptible children may develop chickenpox follow-
ing contact with cases of shingles, but the reverse is unusual.
Symptoms and signs

Mild febrile disease with a rash that comes in crops.
Stages of red spots, then fluid-containing vesicles, pustules -
with much itching - and scabs which fall off without leaving a
scar.
The neck, shoulders and trunk are especially affected.
(7) SMALLPOX (VARIOLA)

One of the recent triumphs of preventive medicine is the virtual
elimination of smallpox throughout the world, through the
successful campaign of the World Health Organization.
Smallpox was a highly infectious and contagious disease
with serious epidemics throughout the centuries causing death
and disfigurement. Now, however, the last report of smallpox
resulting from person-to-person transmission was in Somalia
in 1977 , and 1978 would have been a clear year had two cases of
infection not occurred from a laboratory in Birmingham (UK).
Since the risks of vaccination now outweigh the risks of acquir-
ing the infection, smallpox vaccination is no longer compul-
sory and the number of countries requesting an International
Certificate of Vaccination is gradually declining.
Symptoms and signs

Fever.
Toxaemia and a characteristic rash of spots.
Vesicles and pustules (which swarm with the virus), affecting
the face and trunk.
These might become haemorrhagic leaving scarring. The
victim may die of complicating pneumonia or cardiac failure.
The diagnosis is confirmed by electronmicroscopy recognition

of the virus from the skin lesions.
(8) MUMPS (PAROTITIS)

Mumps is a virus infection of the parotid glands at the angle of
the jaw, and infection is transmitted in the saliva. It is a
relatively trivial infection in children, and epidemics tend to
occur in schools - incubation period is up to 3 weeks.
Symptoms and signs

Fever.
Difficulty in opening the mouth and chewing, with parotid
gland swelling.
The virus may invade the nervous system causing a form of
meningitis.
Complications include orchitis (inflammation of the testis,
usually unilateral) and pancreatitis.
(9) INFLUENZA
Influenza is a virus infection, mainly affecting the upper
respiratory tract.
Symptoms and signs

Cough, sneezing and sore throat.
Fever, headache and limb pains.
Often prostration out of proportion to the respiratory signs.
It is a short, sharp illness (lasting 4-5 days), but in those with
lung disease there is risk of secondary, often staphylococcal
pneumonia.
(10) INFECTIOUS MONONUCLEOSIS (GLANDULAR

FEVER)
This is an acute infection from EB (Epstein-Barr) virus (which
is also found in Burkitt's lymphoma, a glandular swelling in
East African children). Outbreaks of infectious mono-
nucleosis tend to occur in young people living communally.
Symptoms and signs

Sore red throat, often with tonsillar exudate is common, and
distinguishable from streptococcal throat only by the negative
throat swab in glandular fever.
Lymph gland swelling, especially in the neck.
Liver involvement may cause jaundice.
Diagnosis is confirmed by blood film, which shows 'mono-

nuclear' cells - altered lymphocytes, and a positive 'Paul
Bunnell' or 'Monospot' test on the serum.
(11) TUBERCULOSIS
Tuberculosis is due to infection with the tubercle bacillus,
Mycobacterium tuberculosis, termed an 'acid-fast' bacillus as
it resists the decolorizing effect of acid used to stain the
organism for identification under the microscope. It can be
cultured on special media, or if the organisms are scanty,
guinea-pig inoculation (the animal manifesting the infection
after 6 weeks) may establish their presence.
Mode of infection is by inhalation of droplets of infected
sputum into the lungs. A primary focus occurs in the lung
tissue, with involvement of lymph glands near the root of the
lung. When tuberculosis was common, this occurred in most
young people; usually the infection would heal and the subject
become immune to further infection. If resistance was low,
dissemination throughout the body - miliary tuberculosis -
could occur. This might result in tuberculous meningitis,
previously fatal, or chronic infection in bones and kidneys.
Alternatively, the primary infection might become react-
ivated, following a lowered resistance or reinfection, in adult
life, leading to tuberculous pneumonia or to chronic
fibrocaseous tuberculosis of the lungs, with much destruction
cavity formation, and the expectoration of purulent sputum
containing the tubercle bacilli.
Undiagnosed tuberculosis of this type is the present source
of infection.
Symptoms and signs
Cough, sputum, and weight-loss are late signs.
Early recognition depends on chest X-ray. (X-ray is mand-
atory in all undiagnosed fevers, even if chest symptoms are
minimal.)
TB meningitis may present as headache and mild neck stiff-
ness, lumbar puncture showing increased cells, decreased
sugar and the TB bacillus in the spinal fluid.
Diagnosis is confirmed by finding the organism on direct stain-
ing, culture, or guinea-pig inoculation of sputum, cerebro-
spinal fluid, or urine.
(12) BRUCELLOSIS (UNDULANT FEVER)
Cause
Brucella abortus - a small bacterium named after Bruce (who
discovered a similar organism causing Malta fever), and the
tendency of infected cattle to abort their young. Veterinary

surgeons, farmers, and those who drink the milk of infected
animals may contract the disease, which has been eradicated in
some progressive farming countries. Pasteurization is a
measure to render existing milk supplies safe.
Symptoms and signs

Vague ill-health.
Aches and pains.
Fever and night-sweats.
Severe cases may have inflammation of spinal and other joints.
The infection may be acute, or last for months, and should be
considered in any vague pyrexia.
Diagnosis may be confirmed by positive tests for antibodies in

the blood (e.g. agglutination test) and Brucellin skin test.
(13) VENEREAL DISEASE
The venereal diseases are acquired from infected persons at

sexual intercourse, and they have increased in recent years.
The defined venereal diseases are gonorrhoea, syphilis, and
soft chancre, but other sexually transmitted diseases include
non-specific urethritis and some cases of vaginitis from the
trichomonas parasite.
Gonorrhoea
Cause
The gonococcus, a Gram-negative bacterium seen on micro-
scopy, or by culture.
Symptoms and signs

Purulent urethral discharge in males, with dysuria.
Females may have vaginal and urethral discharge, and
infection may involve the ovarian tubes causing sterility, but
many female carriers are symptom-free.
Occasionally there is an acute gonococcal arthritis.
The eyes of newborn babies may be infected from contact with
vaginal secretions at birth.
Syphilis
Cause
A bacterium of spirochaete (corkscrew-like) group called
Treponema pallidum. Like the gonoccocus, the organism fails
to survive outside the body and is acquired only by contact
with an infected lesion, usually at intercourse. There is a delay
of up to a month, during which the treponemes have spread
throughout the body, before signs appear.
Symptoms and signs

Primary stage
A syphilitic sore or chancre on the penis, or the vulva.
Secondary stage
Skin rashes and generalized lymph gland enlargement with
involvement of blood vessels and nervous system - meningo-
vascular syphilis.
Tertiary stage (after a latent period of up to 15 years)

Heart involvement - syphilitic inflammation of the root of the
aorta causing aortic valve incompetence, and dilatation
(aneurysm) of aorta.
Central nervous system
tabes dorsalis (ataxia, shooting pains);
general paralysis of the insane (dementia).
Gumma - abscess-like swelling affecting any organ.
Congenital syphilis occurs from infection in the uterus, the

baby being stillborn or with deformities of brain, teeth and
bones.
Diagnosis
The spirochaete may be seen under the microscope (dark-
ground illumination) in smears from early lesions. Later
DIFFERENTIAL DIAGNOSIS OF COMMON INFECTIONS

Age of onset Distinguishing features
Measles children follows apparent URTI, Koplik's spots in mouth,

confluent erythematous rash
Rubella children/ cervical! occipitallympadenopathy, confluent
young adults rapidly (48 h) clearing rash
Scarlet fever children 'scarlet' rash mainly on trunk, septic throat
Whooping children characteristic inspiratory whoop with paroxysms
cough of coughing
Diphtheria children/non- severely sore throat, grey membrane, severe
immune adults toxaemia and dysphagia, stridor
Chickenpox children/non- separate discrete vesicular spots, arising in crops,
immune adults central in distribution
Smallpox any age vesicles and pustules, some haemorrhagic
centripetal in distribution
Mumps children/ swollen salivary glands and moon face of bilateral
young adults parotitis, accompanying orchitis sometimes and
abdominal pains
Influenza any age prostration and pyrexia disproportionate to the
obvious upper respiratory infection; limb aches
and severe headache
Mononucleosis children/ sore throat and tonsillar exudate with slough,
young adults generalized lymphadenopathy, splenomegaly
and jaundice sometimes
Tuberculosis any age respiratory - chronic productive cough with,
in severe cases, haemoptysis
Brucellosis any age vague, recurrent symptoms including night
sweats and generalized lassitude
Malaria any age/ rigors and severe fever with a pattern of progres-
traveller in sive temperature rise and sweats
exposure area
Key laboratory findings

viral culture possible - diagnosis made by rash
serum antibodies rise
throat swab grows streptococcus

culture of sputum, nasal and throat swabs; cough diagnostic
throat swab, serum antibodies (skin test in immune)
diagnosis by rash - viral culture of vesicle
viral culture of vesicle
salivary swab culture - diagnosis by appearance; serum antibody titre
nasal viral culture; serum antibodies
blood film diagnostic with excess mononuclear cells; antibodies demonstrable;

positive Paul-Bunnell and 'Monospot' test
X-ray diagnostic; sputum culture of acid-fast bacilli and guinea-pig

inoculation; Mantoux skin test
antibody titre rise; Brucellin skin test
parasites seen in fresh stained blood film

diagnosis depends on blood antibody tests, such as the VDRL

(Reference Laboratory), WR (Wasserman reaction) and
treponemal fluorescent antibody and immobilization tests.
Cerebrospinal fluid tests are also necessary in secondary and
tertiary stages.
Non-specific urethritis
This presents as a urethral discharge, from which gonococci
are absent, up to 2 months after sexual intercourse. Some cases
are due to infection with Chlamydia (an organism associated
with the eye disease trachoma in the tropics) but in others the
organism is unknown. There may be associated conjunctivitis
(inflammation of the outer covering of the eye) and arthritis
(lumbar spine and joints of the feet being involved), the
condition called Reiter's syndrome.
(14) MALARIA
Incidence and cause
Malaria is a common tropical disease, and should be
remembered as a cause of fever in travellers from such parts. It
is due to infection with a parasite, of which there are several
types, which undergoes part of its life-cycle in certain
mosquitoes which bite man. The parasite passes from the
salivary glands of the mosquito to the bloodstream of man,
invading the liver and the red blood cells, destruction of the
latter coinciding with the bouts of fever characteristic of the
infection. Native populations develop a natural immunity, and
those carrying the 'sickle cell' trait (from an abnormal haemo-
globin) are protected against severe malaria.
Symptoms and signs

There is a 'cold stage' with shivers and rigors, followed by high
fever with headache and malaise.
The temperature later subsides, with marked sweating.

Diagnosis
Confirmed by finding the parasites in blood films. In severe
cases there may be drowsiness, fits and coma - cerebral
malaria, and sometimes hypotension and collapse, with severe
haemolysis (breakdown of red cells) and darkly pigmented
urine (blackwater fever).
(15) TETANUS
Cause
A bacillus, Clostridium tetani, which inhabits the intestine of
horses and sheep, forming spores found in manure, soil and
dust. The bacillus grows in the absence of oxygen in deep
puncture wounds and injuries - but these may be trivial ones,
or apparently healed. The bacilli produce a toxin which travels
up the peripheral nerves to the central nervous system.
Symptoms and signs

Discomfort and stiffness at the wound, followed by spasm of
the jaw muscles (hence the name lockjaw) within a few days, or
a few weeks, the latter giving a better prognosis.
This is followed by painful general spasms of muscle, precip-
itated by stimuli such as movement or even a loud noise.
These spasms may cause ultimate exhaustion and death.
Index
abscess, extradural 162 underaction 208, 209

acanthosis nigricans 193 virilism 208
acetone 94 adrenal medulla disorders 209,210
in diabetes 199 adverse drug reactions
acetylcholine receptors 182, 183 agranulocytosis 257
achlorhydria 246 barbiturates 189
acid-base balance 227, 228 on bone marrow 247, 257
chart 238, 239 corticosteroids 209
disturbances 234, 235, 240 gold 189
acidosis phenothiazines 160
causes 234, 238 rashes 189
classification 234 tetracyclines 78
investigations 235, 239 age
symptoms 234, 235, 239 and cardiovascular disease 17
acromegaly 210 and tuberculosis 45
acute abdomen 82, 83, 90, 91 agranulocytosis, drug-induced 257
Addison's disease 233 air hunger 39, 235
diagnosis 212, 213 albuminuria 28, 125, 126
investigations 208, 209 alcohol and peptic ulcer 66
symptoms 208 alcoholism 45, 107,272-5
adrenal glands 200 acute dependence 273
disorders and cardiovascular chronic 274, 275
disease 21, 22 and cirrhosis 101
hormones produced 206, 207 incidence 274
overact ion 207 symptoms 274,275
295
aldosterone 22 symptoms 175

function 207 anorexia nervosa 273
and potassium loss 102 antibodies
aldosteronism 207, 208 antinuclear 177
investigations 238, 240 DNA 177
non-respiratory 235, 238 antigen, Australia (HbAg) 99
respiratory cause 235, 238 anuria 118
symptoms 235, 240 differentiation from oliguria
allergy and asthma 46 134, 135
Alzheimer's disease 69 anxiety 269, 270
amoebiasis, features and findings characteristics 276
86,87 difference from depression 276
amylase in pancreatitis 107, 114 277
amyloid disease 125, 127 symptoms 270
anaemia 27,32,69,81,177 aortic coarctation 21
aplastic 245 appendicitis 59
blood formation decrease 245-7 acute, symptoms 59, 82, 83
blood loss 244, 245, 260, 261 pain in 110, 111
bone marrow destruction 247 and vomiting 84, 85
cirrhosis 101 appetite loss 69
definition 243, 244 arterial obstruction
diagnostic chart 260, 261 acute case and symptoms 32, 33
hiatus hernia 65 arteriography 32, 122
incidence 241 arteriosclerosis 24, 31, 140, 162, 268
iron deficiency, causes 245, 260 cerebral arteries 142
laboratory findings 245, 260 in diabetes 199
macrocytic 237 lower limb vessels 32
renal failure 136 arteritis, temporal 158
sideroblastic 220 arthritis
symptoms and signs 243 lumbar spine, symptoms 164
anaemia, haemolytic 247-9, 260, septic, joint pain 180, 181
261 traumatic 180, 181
acquired 248 arthroscopy 172
congenital 247, 260 ascites 90,91, 102
drug-induced 249 causes 91
laboratory findings 261 and hepatic disease 112, 113
microangiopathic 248 laboratory findings 113
plasma defects 248, 249 symptoms 91,113
red cell defects 247, 248 aspirin
symptoms 249 effects of overdose 179
anaemia, pernicious 62, 220, 237, peptic ulcer effects 66, 67
245,246 poisoning 235, 279
cause 245, 260 asthma 37, 46, 47, 188
confirmation tests 246, 261 breathing in 52, 53
symptoms 246, 261 cause of attacks 46
anal fissure 77 extrinsic, precipitating factors
angina pectoris 25 46,47
features 34, 35 intrinsic 47
angiography, cerebral 140, 145 symptoms and signs 47
angioneurotic oedema 41 atelectasis see lung collapse
ankylosing spondylitis 175 atopy 188
and HLA antigens 175 atrial fibrillation 18, 28
INDEX 297
atrial flutter 19 blood tests 62, 243

autoimmune disease 168, 172,203 common infections 282
246, 248, 252 drugs 266
endocrine disorders 195, 196
behaviour liver function 94
in anxiety and depression 277 nutritional disorders 216
disintegration of social 269, 275 and renal function 121
disturbances 266 skeletal disorders 172
beri beri and vitamin B deficiency sugar 200, 201
220 urea levels 136
bile duct blockage 97, 104, 105 blood transfusion mis-match 126
symptoms 105 boils 186
biliary colic 83 bone
pain in 110, III metastatic disease 179
and vomiting 84, 85 rarefaction 178
biliary metabolism 96 scan 179
bilirubin structure 178
detection 94 Bornholm disease 175
excess production 97 botulism 150, 151
toxicity 97 symptoms 151
in urine 119 bowel habits, change in 82
biopsy brain scan, radioisotope 140
bone marrow 241 breathing difficulty, differential
gastric 69 diagnosis chart 52, 53
gastrointestinal 59-61 breathlessness 22, 31
intestinal, technique 75, 76 on waking 27
joint 172 bronchial obstruction 43
liver 95 bronchiectasis 43
muscle 182 cough in 50,51
renal 122, 126 bronchitis, acute 41
blackwater fever 293 bronchitis, chronic 27, 37, 41, 42
bladder disorders causes 42
cancer and haematuria 132, 133 cough in 50, 51
and pain 128 smoking 42
papilloma and haematuria 130, symptoms and signs 42
131 bronchogram, technique 39
blood in bronchiectasis 43
cells 242 bronchopneumonia 41
compOSitIOn 242, 243 bronchoscopy 40
blood disease investigations 243 bronchus
blood gas analysis 40 blocked 49
blood loss carcinoma 49
anaemia symptoms 244 Brucella abortus 287
chronic and iron deficiency 244, brucellosis 287, 288
245 symptoms 288
blood and lymphatic system dis- tests 288
orders 241-63 bulbar palsy 64
common symptoms 241,242 Burkitt's lymphoma 259
examinations 241-3 burns 229
blood pressure
measurement 19,20 calcium
normal 20,21 deficiency 223, 224
sources 223 caruncle of urethra 120

calculi, bladder, urethral and pain CA T see tomography, computerized
128, 129 axial
cancer cellulitis 186
bladder 120, 132, 133 central nervous system infections
colon 77 147-51
gastrointestinal 59 cerebral haemorrhage 23
head of pancreas 97 cerebrospinal fluid (CSF)
large bowel 81, 82 blood-stained 145
large intestine 78 circulation blockage 162
larynx 41 normal pressure 141
liver 103 cerebrovascular accident see stroke
lung 37, 157 cervical spondylitis
ACTH release 48 and headache 159
causes 47, 48 symptoms 163, 164
chest pain 54, 55 chest sounds, inflamed lung 39
complications 48 Cheyne-Stokes breathing 28, 38,
cough in 50, 51 39, 143
malignant growth 47 chicken pox (varicella)
metastases 48 and shingles 150, 284
survival 47 symptoms 284
symptoms and signs 48 chloroform 98
myopathy 182 chlorpromazine 98
oesophagus 64 cholangiography, percutaneous 94
pancreas 107, 114, 115 cholangitis 105
prostate 120 investigations 105
stomach cholecystitis 83
investigations 69 acute, symptoms 104
symptoms and signs 69 chronic 105
vomiting 84, 85 and infection 104
Candida albicans 63, 186,200 pain 110, 111
capillary defects and haemorrhage cholecystography 94, 105
251 cholera
carbon monoxide poisoning 278, features and findings 86, 87
279 potassium loss 232
carbon tetrachloride 97, 98 stools in 73, 78
carcinoma see cancer chronic obstructive airways disease
cardiac arrest see bronchitis, chronic and
causes 25, 26 emphysema
procedure 26 cirrhosis, liver 67,91,100--3,258
cardiac arrhythmia 17 biliary 100
cardiac failure 91 incidence 93
and oedema 23 I investigations 102
and potassium loss 232 laboratory findings and diagnosis
cardiovascular system 17-36 112,113
common disorders 17 portal 100, 112, 113
examinations 17-21 portal, causes and symptoms
mortality 17 101, 102
symptoms 18 post-necrotic 112, 113
c,!ries 63 potassium loss 232
carpal tunnel syndrome 164, 165 Clostridium botulinum 150
symptoms 164, 165 C. tetani 150
INDEX 299
C. welchii 72 causes 229
clotting clinical picture 229, 230
factors 250 input-output chart 230
mechanism 250 investigations 230
clubbing, fingers 38, 43, 48 laboratory findings 135
coagulation defects, causes 253,254 oliguria 134
coeliac disease 74, 76 symptoms 229
collagen diseases 29 delirium tremens 274
colon dementia 268
carcinoma 81, 82 causes 268, 269
disorders 77 senile 268
function 76 symptoms and signs 269
conjunctivitis 41 demyelination 148, 151
connective tissue disease 168, 176 depression 269, 270
erythrocyte sedimentation rate and anxiety, diagnosis 276,277
176 characteristics 276
constipation 76-9 and headache 159
causes 77 symptoms 270
symptoms 77, 78 types 270
copper deposition 101 dermatitis 188, 189
copper and nerve function 225 diabetes 31,32,78, 140, 168
coronary angiogram 26 blood tests 200, 201
coronary artery disease 24-6 causes 196, 197
causes 24 coma 199, 202
investigations 26 complications 199, 200, 202,
mortality 17, 24 203
symptoms 25, 26 findings and diagnosis 212, 213
coronary insufficiency, features glucose tests 200
34,35 incidence 197
corticosteroids and oedema 231 insipidus, polydipsia and polyuria
cortisol overproduction 207 211
cough 38,47 insulin deficiency 196
differential diagnosis chart 50,51 juvenile type I 197, 198
creatine kinase 182 non-insulin dependent type II
Crohn's disease 73, 74, 78 198
fatty stools 74 parathyroid disorders 205, 206
familial 73 symptoms 198, 199
symptoms 73 and thyroid disorders 205, 206
croup 41 virus 197
cushingoid features 48 diagnosis
Cushing's disease 212,213 relevant questions 14
Cushing's syndrome 24,218,231 symptoms, history and examin-
cyanosis 25, 28, 31 ation 15
cystic fibrosis, features and findings diagnostic tap 91
88,89 diarrhoea 78, 79
cystitis 122 acute 78
haematuria in 130, 131 differential diagnosis chart 86-9
pain 128, 129 effects of 79
cystoscopy 122 investigations 79
recurrent 78
defibrination syndrome 253, 254 diastole 20
dehydration diet
and cirrhosis 101 disorders, chart 238, 239

and constipation 77 emphysema 27, 42
vegetarian and anaemia 220 barrel chest 42
digestive system disorders 93-115 breathing in 52, 53
examinations 93-5 bulla 49
symptoms 93 X-ray 53
diphtheria 168 empyema 56, 57
symptoms and toxin 284 encephalitis 147, 148
diverticular disease 78-80 headache 158
and diet 79 encephalomyelitis 147, 148
investigations 80 following infection and vaccin-
pain 110, 111 ation 148
symptoms 79, 80 symptoms 148
dopamine, interference with 160 endocarditis 125
drug dependence (addiction) 272, endocrine-hormonal disorders 195-
275 213
cannabis risks 275 common symptoms 195
opiate abuse 275 diagnostic table 212,213
and withdrawal 275 examination 195, 196
drugs Entamoeba histo/ytica 73
and anaemia 249 enzymes
coagulation defects 253 cardiac 29
haemorrhage 251 elevated in pancreatitis 106, 107
and jaundice 98 serum 94
poisoning 126 epilepsy 137
rashes 189 cause 154
social 13 EEG in 141
dysentery grand mal fits 156, 157
amoebic 73 incidence 155
bacillary, infection 72, 73 idiopathic 155
dysphagia 63,64 investigations 157
causes 64 loss of consciousness 166, 167
dyspnoea, differential diagnosis petit mal diagnosis 155
52,53 symptomatic 154, 155
erysipelas 186
eczema 188, 189 erythema nodosum 81
seborrhoeic 189 erythrocytes
skin rash 190, 191 defects 247
electrocardiogram 20, 21 excess 254
in central chest pain 34, 35 normal count 242
detection of disturbances 21 erythrocyte sedimentation rate (ESR)
pericarditis 29, 30 243,263
and potassium balance 233 Escherichia coli 104, 122
P wave 21 examinations and use of book 9
QRS complex 21 exophthalmos 204
ST segment shifts 30 extrasystole 19
electroencephalogram exudate culture 282
epilepsy 155
grand mal 157 faint, causes and symptoms 153
use of 141 fibrinogen and thrombosis site
electrolyte balance 225-7 detection 36
INDEX 301
fibrinolytic system 250 haematuria 130, 131
fibrositis 175, 176 investigations 124
definition 175 oedema 231
finger-nose test 152 subacute see nephrotic syndrome
fit, epileptic symptoms and causes 124
clonic stage 156 symptoms and laboratory findings
somnolent phase 156, 157 135
tonic stage 156 glossitis 62
fleas 188 glucose tests
fluoride qualitative and quantitative 200
and dental caries 225 glucose tolerance tests 75,201,202
excess 225 gluten enteropathy, features and
folic acid findings 88, 89
supplement in pregnancy 221 glycosuria 196
folic acid deficiency 75, 220, 237, goitre 203; see also thyrotoxicosis
245,247 gonorrhoea
and drugs 219 babies 289
occurrence 221 discharge 288
source 236, 247 gout
food poisoning 71,72 joint pain 181
bacterial causes 71 symptoms 174, 175
Salmonella spp. and 72 tophi 175
Staphylococcus spp. 84-6 and uric acid 174, 181
symptoms growth hormone excess 210
gallstones haematemesis 67, 101, 229

frequency 93 bleeding 68
incidence 104 causes of ulcer complications
symptoms 104 67,68
gangrene 32 haematuria 119, 120
gastrectomy 74 causes 119
gastritis, causes 65 differential diagnosis 130-3
alcoholic and vomiting 84, 85 haemochromatosis 101
gastroenteritis 59 haemoglobinopathies 248
bacterial toxins 70-2 haemophilia
food poisoning, 71,72 factor VIII deficiency 253
gastrointestinal disorders 59-91 sex-linked 253
blind-loops 75 Haemophilus inJluenzae 42
examinations 59,60 haemoptysis 31, 38, 51
infections 78 frothy, bright blood 68
malignant in aged 59 haemorrhage see also subarachnoid
symptoms 60 haemorrhage
visualization 59, 60 capillary defect 251
vomiting 84, 85 clotting factor deficiency 253,
gastroscopy 60, 67 254
german measles see rubella extradural 145
giardiasis 75 intracerebral see stroke
glaucoma, headache in 158 intracranial, symptoms 144, 145
glomerulonephritis 22, 119, 127, and loss of consciousness 166,
177 167
acute 123,130,131,134,135,231 platelet lack 251, 252
chronic 130, 131 subdural 145, 146
haemorrhagic diseases 249-54 cardiac arrhythmias 233, 239

symptoms 250, 251 causes and symptoms 233, 238,
haemorrhoids 78 239
headache 157-9 hypernephroma 120
causes 158, 159 hyperparathyroidism symptoms
mechanism 158 206,223
source 157 hyperpituitarism 212, 213
tension 159 hypertension 17, 21-4, 118, 124,
heart, firing of contraction 20 207
heart block 19 causes, common 22
heart disease causes, rare 21, 22
ischaemic 18 effects of 21
rheumatic 18 essential 22
heart failure 17, 26-9 investigation 23, 24
causes 27 malignant 23
congestive, urinary system 134, retinal examination 140
135 symptoms and signs 22, 23
symptoms 27-9 hypocalcaemia 223
heart sounds, examination 20 effects 224
height/weight tables 61 prolonged 224
hemiplegia 143 hypoglycaemia in diabetes 202
Henoch-Schonlein purpura 124, hypokalaemia
251 cardiac arrhythmias 233, 239
hepatic failure 102, 103 causes 232, 233
hepatitis in disease 232
acute alcoholic 112, 113 extrasystoles 233
B-antigen 99 symptoms 233
cause 98 hypoparathyroidism 205
and cirrhosis 101 symptoms 206
gammaglobulin prophylaxis 99 hypopituitarism 212, 213
non-A, non-B 99 hypoproteinaemia and oedema 231
serum 99 hypothyroidism symptoms and signs
symptoms and signs 99, 100 204,205
viral 102 hysteria 272
hepatolenticular degeneration 101 fits 273
herpes simplex 187
herpes zoster 150, 187 immune complex
hiatus hernia 64, 65 deposition 124
symptoms 65 diseases 125
HLA-B27 175 impetigo 186
Hodgkin's disease 162, 258 indomethacin, adverse effects 66
investigations 262 infarction, definition 25
symptoms and signs 259 infection 29
hormone asthma 46
estimation 195, 196 bacterial of chest 39
sex 207 bronchitis 42
Huntington's chorea 269 Chlamydia 44
hydrocortisone 206 eNS 147-51
hydronephrosis 123 diabetes 200
hypercalcaemia 224 fungal 186, 187
symptoms 225 pneumonia 44
hyperkalaemia 233 and skin rashes 190, 191
INDEX 303
infections, diagnosis of common ketonuria 119
281-93
common symptoms 281,282 lactase deficiency 80
examination 281,282 Landry-Guillain-Barre syndrome
mortality in developed countries 168
281 laparotomy 82
infectious mononucleosis large intestine
outbreaks and symptoms 286 bacterial flora 76
tests 286 function 76
influenza laryngitis
complications 41 acute 41
epidemics 40 breathing 52, 53
and pneumonia 286 chronic 41
symptoms and signs 40, 41, 286 laryngoscopy 40, 41
input-output chart 217 lead poisoning 165
insulin 106 Legionnaire's disease, cause 43
antagonists 197 leprosy 168
function 197, 198 leukaemia 67, 254-7
secretion disorder 196, 197 acute 255
intertrigo 186 causes 255
intervertebral disc prolapse 161 chronic lymphatic 256
intestinal obstruction 83 diagnosis 256
large bowel, pain 108, 109 symptoms 256
small bowel, pain 108, 109 chronic myeloid 255, 256
and vomiting 84, 85 symptoms 256
intracerebral haemorrhage, loss of lymphoblastic 255
consciousness 166, 167 symptoms 255, 256
intracranial pressure leukocytes, normal count 242
headache 158 leukocytosis 51
raised 146 leukopenia 51,87
intravenous pyelogram 24, 121 lice 187, 188
intrinsic factor, lack of 246 crab 188
intussusception 83 nits 187
pain in 108, 109 lipase in pancreatitis 107
iodine deficiency 203 liver
and thyroid function 225 bile secretion 96
IQ (intelligence quotient) 267 cancer 103
iron deficiency 75, 224, 245 cell dysfunction 101
irritable colon syndrome 78 detoxification 96
causes 79 features 95
metabolism and storage 95, 96
jaundice 74, 96-8, 102, 249 poisoning 102
drug-induced 98 liver cell failure
hepatic, causes 97, 98 causes 102, 103
obstructive 98 symptoms 103
post-hepatic 97, 98 liver diseases, metastatic malignant
pre-hepatic 97 112, 113
lockjaw 293
Kernig's sign 147 loss of consciousness, differential
ketoacidosis, diabetic 232, 234 diagnosis 166, 167
symptoms 202 lumbar puncture 141, 162
ketone bodies 198 contraindications 141
multiple sclerosis 152, 153 migraine 137,159

lungs see also respiratory system symptoms 159
abscess 48 mineral deficiency 76, 223-5
and chest pain 54, 55 mitral stenosis 27
alveolar rupture 49 mitral valve disease 27
bellows efficiency 40 mole 192
collapse 48, 49 Molluscum contagiosum 187
patchy collapse 49 mouth, examination 62, 63
lung scanning 31 ulcers 63
lymphatic system see blood and mucorrhoea 88
lymphatic system multiple myeloma, laboratory find-
lymph nodes ings and symptoms 135
disorders 257-9, 262, 263 multiple sclerosis 137,151-3
enlargement, causes 258, 259 cause 151
and infection 259 incidence 151
lymphosarcoma, symptoms and investigations 152, 153
signs 262 symptoms, disseminated 151,152
lysergic acid diethylamide (LSD), mumps 285
effects of 278 and orchitis 285
symptoms 285
magnesium 224 muscular dystrophy 179, 182
malabsorption syndrome 74-6, Duchenne 179, 182
78,219 facio-scapulo-humeral 179
causes 74, 75 investigations 182
investigations 75, 76 limb-girdle 179
symptoms 75 myasthenia gravis 64
malaria 125,248 diagnosis 183
cerebral 293 plasmaphoresis 183
incidence 292 receptor destruction 182
and sickle cell 292 symptoms 183
symptoms 292, 293 Mycobacterium tuberculosis 45,
malignancy, cytology of sputum 39 286
malnutrition 215 urinary 129
and oedema 231 Mycoplasma pneumoniae 44
measles 282, 283 myelitis, transverse 162
symptoms 283 myelography 140, 141
medical history 13-15 myelomatosis 262, 263
melaena 67, 68 investigations 263
causes of ulcer complication 67, symptoms and signs 263
68 myocardial infarction 19,25
melanoma, malignant 192 features 34, 35
meningitis myopathy 179, 182
headache 158 myxoedema 29
loss of consciousness 166, 167 diagnosis 212, 213
symptoms 147 symptoms 205
mental lesion
non-organic 269-72 nephritis and haematuria 130, 131
organic 267-9 nephrotic syndrome 91, 125
mental subnormality 266 investigations 125, 126
assessment 267 oedema 231
mesenteric adenitis 83 nerve conduction studies 141, 142
INDEX 305
nervous system disorders 137-69 vitamin D deficiency in adults 222
common symptoms 138 osteoporosis
examinations 137-42 bone thinning 178
nerve-root 163, 164 symptoms 178, 179
peripheral nerves 164, 165, 168, overhydration symptoms 230
169
pyramidal tract lesions 139 pain
reflexes 138, 139 abdominal 82, 83
upper motor lesions 139 differential diagnosis chart
neuropathy 108-13
alcoholic 168 angina 25
carcinomatous 168 arterial obstruction 33
deficiency 165 central chest, diagnosis chart 54,
and diabetes 199 55
entrapment 164, 165 chest, diagnosis chart 54, 55
peripheral, causes 165, 168, 169 joint, diagnosis 180, 181
symptoms 168, 169 loin 123
toxic 165 musculoskeletal 171
non-specific urethritis 292 peptic ulcer 66, 68
nu tritional system disorders 215-40 urination, diagnosis 128, 129
common symptoms 216 pancreas 105, 106
examinations 215-17 calcification 114
carcinoma 97, 107, 114, 115
obesity 30,215,217-19 symptoms 114, 115
effects of 218,219 diabetes 196
endocrine 218 diseases, incidence and sex 93
genetics 217 scanning 114, 115
metabolic rate 217,218 pancreatitis 83, 88, 89
mortality and life expectancy 219 acute, symptoms 106, 107
overeating 217 chronic, causes 106, 107
psychological 218 enzymes elevated 107
oedema 28, 230-2 pain 110, Ill, 114
clinical presentation 232 symptoms 114
generalized causes 231 and vomiting 84, 85
local causes 231 papilloedema 23, 139
oesophagitis, effects on reflux 64, paracetamol, blood levels in poison-
65 ing 279
oliguria 118 paraesthesiae 235
differential diagnosis 134, 135 paralysis agitans 137
omentum, greater, 'policeman' causes 160
action 90 drug-induced 160
operations 33 idiopathic 160
oral contraceptives 24, 31 symptoms 160, 161
high oestrogen 33 paralytic ileus, treatment 90
and thrush 186 paraplegia 152
ornithosis 44 parathyroid glands
osteoarthritis 173, 174 disorders 205, 206
Jomt pain 180, 181 function 205
joints 173 paratyphoid 70, 71, 78
spinal 174 Parkinson's disease, tongue in 62
symptoms 173 peak expiratory flow rate, normal 40
osteomalacia 75 pellagra 78, 220
peptic ulcer 65-9 pneumonia 37, 41, 49; see also

and acid secretion 66 Legionnaire's disease
causes 66 aspiration 44
complications 67, 68 breathing 52, 53
drugs and 66 broncho- 44
gastric and duodenal 66 chest pain 54, 55
pain 66, 67, 108, 109 cough 50, 51
perforation 68, 69, 83 effects 43
and pain 108, 109 hypostatic 44
pericarditis 29, 30 lobar 44,50,51,56
causes 29 lobar collapse 39
features 34, 35 postoperative 44
symptoms and signs 29,30 symptoms and signs 44, 45
periodontal disease 63 X-ray 53
peripheral artery disease 17, 31 pneumothorax 39, 48, 56
peritonitis breathing 52, 53
symptoms 90 and chest pain 54, 55
vomiting 84, 85 mild 56
pH, metabolic 227 spontaneous 49
phaeochromocytoma 209 tension 56
phenylbutazone and gastric ulcer poliomyelitis, viral spread and symp-
66 toms 149
phenytoin, side-effects of long-term pollution 42
treatment 63 in lung cancer 48
phlebitis 17, 36 polyarteritis nodosa 124
Pick's disease 269 symptoms 177, 178
Pima indians, diabetes 197 polycythaemia 254
pineal gland polymyalgia rheumatica 176
calcified 141,147 polyuria 23, 118
displacement 147 diagnostic chart 134, 135
pituitary-adrenal axis test 211 porphyria 168
pituitary gland disorders portal vein thrombosis, diagnosis
anterior 210,211 112, 113
posterior 211 potassium
underactivity, symptoms 211 disturbances of balance 232,233
plasma effects of 226
composition 243 intake 227
defects 248, 249 loss 227, 232
plasmaphoresis 183 pregnancy 33
platelet ectopic, ruptured 83
aggregation and smoking 250 toxaemia 22 .
functions 249, 250 toxaemia, oedema 231
lack 251, 252 urinary system 134, 135
pleural effusion 48 proteinuria occurrence 119
causes 56 prothrombin
investigations 57 and coagulation 250
pain 56 deficiency 223, 253
pleurisy 56, 57 psittacosis 44
chest pain 54, 55 psoriasis
pleural rub 39 and arthropathy 191, 192
Pneumococcus (Streptococcus) recognition 192
pneumoniae 42 skin rashes 190, 191
INDEX 307
psychological system disorders renal colic 83
265-79 renal failure, acute, symptoms and
common symptoms 265 causes 126
examinations 265, 266 renal failure, chronic
and hospitalization 265 causes 127
incidence 265 in diabetes 199
psychological tests 266 investigations 136
psychopathic disorders 272 occurrence 127
psychoses 270--2 symptoms 127, 136
symptoms 271 urinary system 134, 135
psychosomatic disorders 272, 273 renal function tests
symptoms 273 blood urea 121
pulmonary angiography 31 clearance tests 121
pulmonary embolism 49 urine concentration 121
causes 30, 31 renal infarction 119
features 34, 35 renin 22
massive, effects 31 respiration rate 38, 39
pulmonary infarction 31,49,56 respiratory disorders 37-57
pulse rate and rhythm examinations 37
cardiovascular disease 18, 19 frequency 37
heart failure 28 influenza 41
in peptic ulcer 68 mortality 37
purgative abuse 77 symptoms 38
purpura 67, 119,251 respiratory infection 27
anaphylactoid see Henoch-Schon- rest pain 32
lein purpura reticuloses 259, 262, 263
pyelography, retrograde 122 retina, examination 139, 140
pyelonephritis 22, 127 retinopathy in diabetes 199
acute 122 rhesus factor 248, 249
chronic 123 rheumatic fever 29
and haematuria 130, 131 rheumatoid arthritis 29, 171-3
symptoms 122, 123 cause 172
pyloric spasm 68, 69 incidence 172
pain in 69 investigations 173
pyloric stenosis, pain 69 joint pain 180, 181
pyramidal tract in multiple sclerosis symptoms 173
152 rheumatoid factor 173
rickets 222
rabies, transmission and symptoms Rose-Waaler test 173
149 rubella symptoms 283
radial nerve trauma 165
Raynaud's syndrome 33 Salmonella spp. in typhoid and para-
rectum, carcinoma 81,82 typhoid 70,71
reflexes, examination of 138, 139 salmonellosis, features and findings
knee jerk 138 86,87
and muscle weakness 138 salpingitis 83
regional enteritis, features and find- salt
ings 86,87 depletion, effects 228, 229
Reiter's syndrome 292 excess intake 227
renal artery stenosis 22 requirement 226
renal calculi and haematuria 132, scabies 188
133 mites 186
scarlet fever, bacterial toxin 283 effects 146

schistosomiasis 120 X-ray confirmation 147, 167
schizophrenia 268, 270-2 sphygmomanometer, use of 19
symptoms 271 spinal cord damage
SCiatIca 164, 174 causes 161, 162
scleroderma 33 compression 161, 162
scurvy 63, 221 investigations 162
self-poisoning (suicide attempts) localization 162
278 spirometry 40
Shigella sonnei dysentery 72 spleen
shigellosis, features and findings enlargement, causes 258
86,87 function 257, 258
shingles 149, 150, 187 septic 258
dormant virus 150 splenomegaly, effects 258
symptoms 150 splenoportography 113
sickle cell disease 248 sprue, features and findings 88, 89
sigmoidoscopy 79, 81, 82, 87 sputum
procto- 113 in asthma 47
sino-atrial disease 154 and diagnosis of cough 50, 51
sinus arrhythmia 18 examination of purulent 39
sinusitis headache 158 lung abscess 55
skeletal system disorders 171-83 staphylococcal enterocolitis, features
common symptoms 171 and findings 86, 87
examinations 171, 172 status asthmaticus 47
skin status epilepticus 157
appearance in arteriosclerosis 32 steatorrhoea 88
colour in cirrhosis IOI faecal fat output 75
in renal failure 136 steroids
skin disorders 185-93 side-effects 209
common symptoms 185 synthetic 209
examination 185 Stokes-Adams attacks 154
incidence 185 stomatitis 63
infections 186, 187 stools
infestations 187, 188 bacteriology 62, 79, 81, 82
rashes and diagnosis 190, 191 fat 79
tumours 192, 193 hepatitis 100
small intestine, function 70 occult blood 69, 79
smallpox 284, 285 pea soup 71
eradication _284, 285 viral culture 148
scarring 285 strokes 142-4
symptoms 285 effects 142, 143
smoking 24, 31 mortality 137
and bronchitis 42 suddenness 144
carcinogens 47 symptoms and signs 143, 144
furred tongue 62 subarachnoid haemorrhage 140,
and lung cancer 47 141
and platelets 250 development defect 144
sodium, functions of 226 loss of consciousness 166, 167
sore throat 41 suicide 265
space-occupying lesions of brain attempted 278, 279
146, 147 symptoms, use of IO
causes 146 syncope 18, 153, 154
INDEX 309
cardiac 154 Treponema pallidum 289
carotid-sinus 154 tests 292
cough 154 TRH test 204
loss of consciousness 166, 167 triorthocresyl phosphate 265
syphilis tropical sprue 74
congenital 289 tuberculin test 51
diagnosis 289, 292 tuberculosis
stages 289 meningitis 287
systemic lupus erythematosus 124, miliary 287
127 mode of infection 287
butterfly rash 176, 177 symptoms 287
investigations 177 tuberculosis, pulmonary 45,46,48
symptoms 16, 177 causes 45
systole 20 cough 50,51
reservoirs 45
symptoms 45,46
tachycardia, paroxysmal 18 tuberculosis, urinary tract 123
tenesmus 81, 86 pain 128, 129
tetanus tumour 209
cause, bacterial 293 acoustic neuroma 146
deep wounds 150 adrenal 22
symptoms 150 biopsy 61
thalassaemia 248 bladder 128, 129
thrombocytopenic purpura, causes cerebral 269
251,252 and loss of consciousness
thrush 63 166, 167
mouth and vagina 186 headache 158
thyroiditis, Hashimoto's 205 neurofibroma 16
thyrotoxicosis 18, 78 pancreas 33
common in women 203 typhoid 70, 71, 78
diagnosis 212,213 systemic symptoms 71
investigations 204
symptoms and signs 203,204 ulcer see also peptic ulcer
thyroxine estimation 204 obstructed 84, 85
tinea 186, 187 ulcerative colitis 78, 80, 81
tomogram 39 complication 81
tomography, computerized axial features and findings 86, 87
(CAT) 140, 145 investigations 81
tongue examination 62 laboratory findings 113
toxic confusional state 267 pain 112, 113
symptoms 268 possible causes 80
toxin symptoms and signs 80, 81
liver necrosis 102 ultrasonic scanning 30
nitrogenous 103 liver and biliary tract 94
staphylococcal 72, 283 pancreas 114
tetanus 150 portable detector 36
tracheitis uraemia and renal failure 127
acute causes 41 urethritis
breathing 52, 53 haematuria 130, 131
tracheobronchitis 5 pain and symptoms 129
coughin 50,51 urinary system disorders 117-36
tremor 160, 161 examinations 117-22
symptoms 117, 118 hepatitis 98-100

trauma and haematuria 130,131 pneumonia 43,44
urinary tract infections 120, 122 rashes 190, 191
123, 129 skin 187
and bacteria 122 virus
urinary tract stones, symptoms and Coxsackie 175, 197
signs 123 Epstein-Barr 286
urine herpes simplex 148-50
acetone 119 polio 149
acidity 118 vitamin
blood 119,120 absorption of fat soluble 96
colour 118 deficiencies 215,219-23
concentration tests 121 chart of 236, 237
cytology 120 vitamin A (retinol) deficiency 219,
deposits 118 237
examination 118-20 sources 236
ketosteroids 208 vitamin B
microscopy 120 deficiency 62, 75, 78, 165, 168,
midstream 120 220,274
protein 119 in alcoholics 220
specific gravity 121 sources 220, 236
specimens for bacteriology 120 types 219
sugar 118 vitamin B 12 in pernicious anaemia
volume 118 246
urine tests vitamin C
digestive system disorders 94 deficiency 63,221,237,251
drugs 226 potatoes 221
endocrine disorders 196 source 221
nutritional factors 216 vitamin D2 (calciferol)
and renal function 121 added to margarine 221
urobilinogen 94, 97 formation 222
urochrome 118 vitamin D3 (cholecalciferol) 221
urticaria 189, 192,251 requirements 222
diagnosis 190,191 vitamin D deficiency 75, 178, 237
rash 190,191 causes 222
intoxication 224
varicose veins 17, 77 states 222, 236
vasopressin, lack 211 vitamin E
vena cava, obstruction, effects of sources 222, 236
48 deficiency 223,237
veneral disease 288, 290, 292 vitamin K
transmission 228 absorption and bruising 98, 253
venography, portal 94 deficiency 75, 223, 237
venous thrombosis 29 liver requirement 95
causes 33 source 223, 236
deep vein 33, 36 vomiting and gastrointestinal dis-
and pulmonary embolism 30 orders 84, 85
ventricular fibrillation 25
viral infection 29; see also indi- warts 187
vidual diseases water
brain 147, 148 deficiency, effects 228,234
enteritic, features 86, 87 input-output 225
INDEX 311
requirements 225 gastrointestinal, contraindic-
weight ations 59, 60
fat proportion 216 hiatus hernia 65
loss 48, 60, 69, 89, 103, 204 hypertension 24
standard tables 60, 61 joints and bone 172,181
whooping cough 43,283,284 kidneys 121, 122, 136
diagnosis 50,51 lung collapse 49
symptoms 283 ossification 216
Widal agglutination test 71 pancreas 114
peptic ulcer 67, 68, 109
pleurisy 57
X-ray renal calculi 133
bowel 89, 109, 111 respiratory system 39
chest 140 skull 140,167,213
coronary artery disease 26 spondylosis 164
cough 50,51 tuberculosis 45, 287
digestive system 94 venography 36
dysphagia 64 and vomiting 85
dyspnoea 64 urinary system 117, 121, 122, 129
gallstones 104 xylose tolerance test 75

Differential Diagnosis

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Differential Diagnosis

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Differential

Copyright © 1981 A. D. G. Gunn

First published 1981

All rights reserved. No part of this publication

British Library Cataloguing in Publication Data

ISBN-13: 978-94-009-8062-4 e-ISBN -13: 978-94-009-8060-0

Central chest pain 34

This book is designed for use by medical students, nurses,

iated. Finally without the stimulus and encouragement of

A guide to differential diagnosis, unless it ran to several

relevant literature. This book, therefore, is a guide, logically

Taking a medical history is a skill, acquired by most as a result

There are, however, only two questions that require answering

The commonest disorders of the cardiovascular system are

Diagnosis of disorder will depend on symptoms, history,

Common symptoms of generalized disorder will be:

(A) EXAMINATION OF THE PULSE

The atria are twitching rapidly and irregularly at around

(B) EXAMINATION OF THE BLOOD PRESSURE

fat arm causes a falsely high reading. The normal blood

A falling blood pressure indicates haemorrhage or deteriorat-

(C) EXAMINATION OF THE HEART SOUNDS

Common Disorders of the Cardiovascular

Tumour of medulla, producing adrenaline-like substances

Symptoms and signs

Headache is not a common complaint except in severe hyper-

These effects of hypertension may be very gradual, with pro-

ment, may contain albumin; laboratory examination

(2) CORONARY ARTERY DISEASE

Myocardial infarction (heart attack)

all its movements ceasing. In both cases there is a sudden

(3) HEART FAILURE

This may occur acutely, after massive myocardial infarction,

Symptoms and signs

oedema causes extreme breathlessness and the production of

Lack of appetite, nausea and vomiting - occur from conges-

Urinary output - may be lowered from poor circulation to the

Symptoms and signs

1:1- ::i.;, ' ~ ±

H~t It: ~ lIlt .:1 h.- ...

Electrocardiogram showing ST segment shifts

ventricular failure - distended neck veins, enlarged liver and

(5) PULMONARY EMBOLISM

Pulmonary infarction - pain on breathing, from pleural

Massive pulmonary embolus - a large clot may completely

(6) PERIPHERAL ARTERIAL AND VASCULAR DISEASE

Symptoms and signs

ACUTE ARTERIAL OBSTRUCTION

VENOUS THROMBOSIS AND EMBOLISM

DIFFERENTIAL DIAGNOSIS OF CENTRAL CHEST PAIN

Angina pressing substernal shoulders, usually

Coronary pressing, substernal shoulders, few

Myocardial pressing substernal shoulders, less than

Acute crushing or substernal shoulders, days to

Pulmonary sudden and substernal chest, minutes

Onset Associated signs EeG changes

exertion; fear and anxiety; ECO may show ST

usually at fear and anxiety; ECO may show ST and T

usually at fear and anxiety; Q waves and other

usually at fever; non-productive ST elevation and T

usually at marked dyspnoea; rapid shift of QRS axis to

Symptoms and signs

Superficial vein thrombosis (phlebitis)